Search PubMed⌕ Search

Biomedical subjects

B Lacour

Publications and source records attributed to B Lacour.

At least 91 records · Page 5Linked to original sources
PubMed1995

[Handicaps and the perinatal period. II. Perinatal pathology and severe deficiencies].

BACKGROUND: In the last two decades, the infant mortality rate has dramatically declined. But improved management of newborns may induce an increased prevalence of neurodevelopmental handicaps. The aim of this paper is to estimate the rate of major disabilities and their relationships to perinatal events. POPULATION AND METHODS: Three hundred and sixteen children born in 1984 and registered by the "Commission Départementale de l'Education Spéciale" (CDES) were included in the study. Among these, 97 had either cerebral palsy, blindness, deafness, or mental retardation. These 97 children were compared to 602 school age controls using a multivariate analysis (logistic regression). RESULTS: The rate of major disabilities among the 6-year old children is 3.4/1000. It was 5/1000 in 1972 and 4.3/1000 in 1976. This frequency is higher in the children who were preterm (odds ratio--OR = 4.8), small for gestational age (OR = 3.3) or suffered from perinatal asphyxia (OR = 32.8). These three factors accounted for 37.4% of major disabilities. CONCLUSION: This study emphasizes the relationships between perinatal events and some major handicaps but also shows that antenatal factors may be involved in neurodevelopmental problems.

Asphyxia Neonatorum↗
PubMed1995

Parathyroidectomy does not prevent the renal PTH/PTHrP receptor down-regulation in uremic rats.

In a recent study we demonstrated that the PTH/PTHrP receptor (PTH-R) mRNA was markedly down-regulated in the remnant kidney of uremic rats with severe secondary hyperparathyroidism. Among the factors potentially implicated in this down-regulation, to date only PTH has been demonstrated to modulate PTH-R expression. Here, we examined the effect of thyroparathyroidectomy (TPTX) on the renal expression of PTH-R in rats with normal renal function or with chronic renal failure (CRF) induced by 5/6 nephrectomy. Four groups of rats were studied: control, TPTX, CRF, and CRF + TPTX. Moderate-degree renal failure was documented by mean (+/- SD) creatinine clearances (microliter/min/100 g body wt) of 259 +/- 40 and 212 +/- 45 in CRF and CRF + TPTX rats, compared with 646 +/- 123 and 511 +/- 156 in control and TPTX rats, respectively. Plasma phosphorus, calcitriol, and ionized calcium were significantly lower in CRF and CRF + TPTX than in control animals. Plasma ionized calcium and calcitriol were also lower in TPTX than in control rats. Plasma PTH levels (pg/ml) were increased in CRF rats (41.8 +/- 29.4), and markedly decreased in TPTX (10.1 +/- 7.8) and CRF + TPTX (8.0 +/- 3.8) rats compared with control rats (21.7 +/- 7.5). Northern blot analysis showed that the level of the steady-state PTH-R mRNA in the kidney of CRF and CRF + TPTX rats was markedly decreased compared with that of control rats, the ratios of PTH-R mRNA/beta-actin mRNA being 0.28 +/- 0.04 and 0.27 +/- 0.03 versus 0.54 +/- 0.05, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗
PubMed1995

Enhanced detection of hematogenous circulating prostatic cells in patients with prostate adenocarcinoma by using nested reverse transcription polymerase chain reaction assay based on prostate-specific membrane antigen.

We report the development of a new sensitive nested reverse transcription-polymerase chain reaction (RT-PCR) assay, using primers derived from the prostate-specific membrane antigen (PSM) cDNA sequence, to detect an hematogenous spread of prostate adenocarcinoma cells. In 60 patients with a biopsy-proven prostate cancer, PSM and PSA RT-PCR detected circulating prostate cells in 40 and 20 patients, respectively. In pT4 M+ and pT3 M+ disease patients, nested PSM primers detected cells in 28 of 33 patients (85%), whereas nested PSA primers detected cells in 17 of 33 (51%). In patients with organ-confined cancer spread (pT2a and pT2b patients) before radical prostatectomy, nested PSM RT-PCR detected circulating prostatic epithelial cells in 6 of 17 patients (35%), which suggests that an hematogenous spread of prostate cells may occur early in prostate cancer history. Altogether, these results suggest that the detection of PSM-expressing cells in blood may predict the development of cancer in patients without clinically apparent prostate cancer. Nevertheless, the potential application and the clinical significance of detection of hematogenous prostate cells through the use of nested PSM primers need an extensive longitudinal study.

Adenocarcinoma↗
PubMed1995

Stimulating effects of sorbitol and L-xylose on rat ileal Ca transport in vitro.

The direct effect of sorbitol and L-xylose on net intestinal calcium transport was compared to that of lactose, by determining unidirectional steady state calcium fluxes in segments of rat ileum in vitro under short-circuited conditions. The iso-molar addition of either 100 mM sorbitol, L-xylose, or lactose in mucosal buffer fluid increased the absorptive flux of Ca from mucosa to serosa to a similar extent and thus reversed ileal net Ca transport from net secretion to a zero net movement. The three substances decreased tissue conductance and reversed tissue polarity. At 200 mM, sorbitol induced a stimulation of net Ca transport due to an enhancement of absorptive Ca flux but in addition due to a decrease of secretory Ca flux from serosa to mucosa. The presence of 1 mM N-ethylmaleimide abolished the effects of sorbitol on ileal Ca flux. In conclusion, the present result shows that sorbitol, L-xylose, and lactose increase net Ca absorption to a comparable extent, in the absence of electrochemical or osmotic gradients. Such an absence of specificity suggests a stimulation of transcellular Ca transport related to the decrease of Na concentration in mucosal solution.

Animals↗
PubMed1994

Stimulation of ileal calcium absorption by sorbitol, L-xylose, or creatine via a decrease in luminal sodium concentration: relation with concomitant changes in enterocyte energy metabolism.

Ligated ileal loops, 30 cm in length, of 4-month-old male Wistar rats were instilled with 3 ml of a 10 mM CaCl2 solution (added with 0.25 muCi 45Ca) in the absence (control) or presence of 100mM sorbitol, L-xylose, or creatine. Ileal calcium (Ca) transport, measured by plasma 45Ca appearance, was found to be similar 30 minutes after fluid instillation in all four instances. However, thereafter, 45Ca appearance in plasma did not increase further in control animals whereas it increased twice as much during the subsequent 30 minutes in the presence of sorbitol, L-xylose, or creatine. However, when loops of similar length were instilled with only 1.0 ml of such solutions, the sorbitol effect was already observed during the first 30 minutes. The stimulation of ileal Ca absorption induced by the presence of sorbitol appeared to be due to a cellular effect, associated with a decreased flux across the paracellular pathway, as indicated by 3H-mannitol absorption. The presence of sorbitol in instilled ileal solution induced a significant decrease in luminal Na, K, bicarbonate, and Cl concentrations at each time point studied (30, 60, 120, or 240 minutes after instillation). Thirty minutes after instillation, no difference in soluble Ca concentration was observed between control and experimental rats. After 60 minutes, Ca concentration was dramatically decreased in control rats but it remained nearly constant in experimental animals. Thus, the presence of substances enhancing ileal Ca transport favored the maintenance of soluble Ca in ileal solution during longer time periods than their absence. In the ileal enterocyte, these substances induced a twofold increase of ATP content compared with controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗
PubMed1994

Reduced inhibitory activity of uronic-acid-rich protein in urine of stone formers.

We recently reported that human urine contains a newly identified urinary glycoprotein acting as a potent inhibitor against calcium oxalate crystallization. This inhibitor is a uronic-acid-rich protein (UAP) with a molecular weight of approximately 35 kDa. In the present study, UAP was isolated from urine of stone formers and of subjects without a stone history, and its inhibitory activity was tested in a calcium oxalate crystallization system in vitro. Our results show a weaker inhibitory activity of UAP extracted from the urine of stone formers than that extracted from the urine of healthy subjects. Preliminary analyses of amino acid and carbohydrate content showed some differences between the two groups. The main difference was the reduction in sialic acid in UAP isolated from the urine of stone formers. We suggest that UAP contributes significantly to total urinary inhibitory activity of calcium oxalate crystallization and that the decrease in this activity in the urine of recurrent stone formers is due, in part, to the weak inhibitory activity of UAP. A structural abnormality of UAP could explain the diminution of its inhibitory activity in the urine of stone formers.

Adult↗
PubMed1994

Physiological correlates of attenuated salt appetite in Fischer 344 rats.

Dietary NaCl deprivation stimulates a robust salt appetite in Wistar rats but has little influence on this behavior in rats of the Fischer 344 (F344) strain. To examine physiological substrates of attenuated salt appetite in F344 rats, several pertinent measures of renal function and fluid homeostasis were made in Wistar and F344 rats eating normal and NaCl-deplete diets. Physiological adjustments to NaCl deprivation were similar between the two strains; however, F344 rats showed smaller increases in plasma renin activity (PRA) than their Wistar counterparts. In addition, F344s decreased urinary sodium excretion more rapidly than Wistar rats in response to deprivation. The present studies also revealed several strain differences in baseline fluid and electrolyte regulation. Relative to the Wistar strain, F344 rats were characterized by high baseline PRA, increased arginine vasopressin (AVP) excretion, decreased urine volume, and diminished thirst. We propose that AVP and oxytocin activation may reduce salt preference and suppress the development of salt appetite in F344 rats.

Animals↗
PubMed1994

Opposite renal effects of a PGE1 analog and prostacyclin in humans.

Renal effects of prostaglandins have been widely investigated in anesthetized animals, but in contrast only few studies have been devoted to healthy and diseased humans. Recently, both prostacyclin and a stable analog of PGE1, misoprostol, have been available for therapeutic purposes in clinical conditions associated with peripheral or renal vasoconstriction; however, the renal effects have not been defined. We have therefore studied the acute renal effects of PGI2 5 ng.kg/min intravenously and of misoprostol, a stable PGE1 analogue, 400 micrograms orally in two groups of respectively 8 and 12 healthy supine subjects on normal sodium diet using sodium, lithium, inulin, PAH and neutral dextran clearances. PGI2 induced a slight natriuretic effect, a systemic and renal vasodilation with a decrease in mean arterial pressure from 85.3 +/- 1.1 to 80.2 +/- 1.6 mm Hg (P < 0.01) and in renal vascular resistance from 94 +/- 6 to 75 +/- 5 mm Hg.min/ml (P < 0.001). GFR did not change whereas fractional clearance of dextran decreased over the 34 to 48 A radius range. Applying these changes on a hydrodynamic model of filtration of macromolecules through water-filled pores, we calculated that PGI2 decreased the glomerular transcapillary pressure gradient from 35 +/- 1 to 32 +/- 1 mm Hg (P < 0.001), decreased nonsignificantly the ultrafiltration coefficient Kf and did not affect the membrane parameters r0 and omega 0. Misoprostol had no natriuretic effect, induced slight renal vasoconstriction and moderate decrease in GFR from 124 +/- 9 to 114 +/- 10 ml/min.1.73 m2 (P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1994

The renal PTH/PTHrP receptor is down-regulated in rats with chronic renal failure.

Hypocalcemia, hyperphosphatemia, and resistance to the action of PTH are well characterized features in the setting of advanced chronic renal failure (CRF). Although the underlying mechanisms are ill-understood, clinical and experimental evidence points to both PTH receptor down-regulation and post-receptor abnormalities in their pathogenesis. In the present study we have examined the effect of advanced CRF in rats on the renal expression of PTH/PTHrP receptor (PTH-R). CRF was created by a standard two-step operation (5/6 nephrectomy). Four weeks thereafter, 19 uremic rats were compared with 23 sham-operated rats. Uremic rats had higher mean (+/- SD) plasma creatinine levels than control rats, 164 +/- 107 microM versus 43 +/- 5 microM, respectively. They also had higher plasma phosphorus and iPTH levels, 4.70 +/- 1.71 mM versus 2.59 +/- 0.37 mM and 561 +/- 336 versus 27 +/- 18 pg/ml, respectively. Mean plasma total calcium and blood ionized calcium were significantly lower in uremic than in control rats, 2.13 +/- 0.06 mM versus 2.61 +/- 0.10 mM and 1.07 +/- 0.11 versus 1.31 +/- 0.06 mM, respectively. Mean plasma calcitriol concentration was also significantly lower in uremic than in control rats, 39.8 +/- 14.6 and 80.4 +/- 15.2 pg/ml, respectively. Nine out of the 19 rats were examined for renal PTH-R gene expression.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗
PubMed1994

Platelet membrane microviscosity in Sabra rats with early salt hypertension.

1. To investigate the possibility that arterial hypertension is associated with changes in the physicochemical properties of cell membranes, we have studied the effects of dietary salt loading on platelet membrane microviscosity in hypertension-prone and -resistant Sabra rats. 2. Sixteen hypertension-prone and 14 hypertension-resistant Sabra rats were submitted to either a low-salt (0.25% NaCl) or a high-salt (4% NaCl) diet for 3-4 weeks. Platelet membrane anisotropy was determined, in the presence and absence of extracellular Na+, using two fluorescent probes, diphenylhexatriene and trimethylamino-diphenylhexatriene, inserted in different areas of the cell membranes. 3. A decrease in diphenylhexatriene anisotropy was demonstrated when platelets of hypertension-prone (but not hypertension-resistant) Sabra rats were suspended in a Na(+)-free medium. This alteration in membrane dynamic properties is localized within the hydrophobic core of the platelet membranes and is independent of salt intake. It reflects an abnormal fluidizing effect of extracellular Na+ removal. 4. Platelets of hypertension-prone and hypertension-resistant Sabra rats did not differ significantly in trimethylamino-diphenylhexatriene fluorescence anisotropy, irrespective of the incubation media used. Extracellular Na+ removal caused an increase in trimethylamino-diphenylhexatriene fluorescence anisotropy in all groups, the change being greatest in salt-loaded rats. 5. This study indicates that platelet membrane microviscosity is specifically altered in the hypertension-prone Sabra rat irrespective of salt intake. This raises the question of the relation of this inherited defect with the susceptibility of this strain to dietary salt loading.

Animals↗
PubMed1994

Influence of various calcium intakes on calcium-oxalate crystalluria in rats on sodium-oxalate diet.

Forty adult male Wistar rats were placed in metabolic cages on a Ca-deficient diet (0.1%) for 7 days and then on a Ca-deficient, Na-oxalate (NaOx) enriched diet (20 mg/100 g) for another 14 days. The animals were subdivided into three groups receiving three different types of mineral water: group I (n = 13), Badoit (Ca 222 mg/l); group II (n = 14), Contrexéville (Ca 467 mg/l); and group III (n = 13), Evian (Ca 78 mg/l). Another series of 25 rats (group I, n = 9; group II, n = 8; group III, n = 8) underwent the same study protocol, except that they received a normal Ca diet (1%). On the low-Ca diet, urinary Ca-Ox monohydrate (COM) crystals were observed only under the Na-Ox diet, with a mean crystal number significantly greater in group III (16.7 +/- 4.5 crystals/mm3) than in group I or II rats (2.5 +/- 1.5 or 4.1 +/- 1.5 crystals/mm3, respectively). Urinary Ca concentrations decreased in all groups (P < 0.001) under the Na-Ox diet, while urinary oxalate concentrations increased in all groups (P < 0.001). On the normal Ca diet, COM crystal excretion was observed only with the Na-Ox-enriched diet, but in this case feeding the Na-Ox diet did not modify urinary oxalate excretion. Ca/Ox ratio was significantly lower under 0.1% Ca diet than under normal Ca diet, related with the type and the number of crystals observed, demonstrating that assessment of crystalluria can provide an index of disease severity. Moreover, the hardness of the drinking water influences urinary COM crystal excretion only under a low-Ca, oxalate-rich diet, suggesting that the total calcium intake rather than the water calcium content is an important factor in the occurrence of Ca-Ox nephrolithiasis.

Animals↗
PubMed1994

Hyperhomocysteinaemia: a significant risk factor for cardiovascular disease in renal transplant recipients.

Moderate hyperhomocysteinaemia has been shown to constitute an independent risk factor for cardiovascular disease (CVD), a frequent cause of morbidity and mortality in renal transplant recipients (RTR). In these patients few data regarding both total homocysteine levels and their influence on cardiovascular risk have been reported. We therefore studied serum homocysteine levels in deep-frozen sera from 42 kidney transplant recipients with a follow-up of 11 +/- 4.5 years (mean +/- SD) after transplantation. Eighteen patients had one or more ischaemic events (CVD (+)) and 24 patients had none (CVD (-)). Serum samples had been drawn 1-6 months prior to the first vascular event in CVD (+) patients and serum storage time was comparable in both CVD (-) and CVD (+) patients. Serum homocysteine levels were measured using a radioenzymatic method. Mean homocysteine level was significantly higher in 42 RTR males and females (15.5 +/- 6.3, 13.5 +/- 5.5 microM respectively) compared with 35 control subjects matched for age and sex (8.7 +/- 1.9, 7.5 +/- 1.9 microM, P < 0.001). The difference in serum homocysteine levels between CVD (+) and CVD (-) RTR nearly reached statistical significance in male patients (18.6 +/- 7.8 versus 13.1 +/- 3.4 microM, P < 0.06) but not in female patients (P = NS). In the CVD (+) group 11/18 patients had homocysteine levels > 14 microM (the upper limit in healthy controls) versus 7/24 in the CVD (-) group (P = 0.04). In these patients we simultaneously measured in the same serum samples, serum triglycerides, and total and HDL cholesterol, and calculated LDL cholesterol. By stepwise discriminant analysis and by logistic regression analysis in this relatively small patient population, only serum triglycerides and homocysteine were selected as risk factors associated with CVD. We conclude that significant hyperhomocysteinaemia is present in renal transplant recipients and represents a potential risk factor for cardiovascular disease in these patients.

Adult↗
PubMed1994

Acute renal effects of neutral endopeptidase inhibition in humans.

The acute renal effects of neutral endopeptidase 24.11 (E-24.11) inhibition induced by a single oral dose of sinorphan (100 mg) were investigated in 10 healthy normotensive subjects on normal sodium diet. Sinorphan inhibited 90% of E-24.11 activity and increased plasma atrial natriuretic peptide (ANP) and urinary guanosine 3',5'-cyclic monophosphate (cGMP) by 70 and 100%, respectively. Sinorphan increased urinary sodium output by 50% (P < 0.001) and decreased fractional distal reabsorption by 4% (P < 0.01). Sinorphan increased glomerular filtration rate (GFR) and filtration fraction by 10% 1 h after administration and decreased renal plasma flow by 10%. Mean arterial pressure, renal vascular resistance, plasma aldosterone concentration, and renin activity were unmodified. Sinorphan decreased fractional clearance of neutral dextrans over the 34- to 52-A radius range. Applying the changes along with a hydrodynamic isopore with shunt model, sinorphan significantly increased capillary pressure gradient (delta P; 39 +/- 1 vs. 34 +/- 1 mmHg; P < 0.01), whereas ultrafiltration coefficient was unchanged. In conclusion, endopeptidase inhibition increased endogenous plasma ANP and cGMP generation and induced natriuresis through both an increase in filtered load and a decrease in distal tubular reabsorption of sodium. Sinorphan increases GFR, filtration fraction, and delta P, probably through an increase in efferent over afferent arteriolar resistance ratio.

Blood Pressure↗
PubMed1994

[In vitro effect of citrate and phosphates on calcium transport in the rat ileum].

OBJECTIVES AND METHODS: The effect of the presence of phosphates or citrate on ileal calcium (Ca) absorption was studied by using rat ileum mounted in a Ussing chamber. RESULTS: Mucosa-to-serosa and serosa-to-mucosa undirectional fluxes were not modified by mucosal addition of 2.8 mM Na phosphate or 2.0 mM Na citrate to Krebs-Ringer-bicarbonate buffer containing 1.25 mM CaCl2. However, 50 mM Na citrate induced a significant and similar increase of both unidirectional Ca fluxes, leading to no modification of net Ca flux. This high citrate concentration was associated with a significant increase of tissue conductance and no alteration of zona adherens and tight junction as observed by electron microscopy. CONCLUSIONS: Thus in the absence of any Ca gradient along the epithelium, even at high concentration, citrate did not induced modification of ileal Ca absorption.

Animals↗
PubMed1994

Duodenal calcium binding protein and active calcium transport in rats: are they functionally related?

The effects of calcitriol and a novel calcitriol analogue, 22-oxacalcitriol (OCT) on duodenal Ca transport, calbindin-D9k mRNA, and calbindin-D9k content were studied in two animal models reflecting common human pathologies, namely arterial hypertension and chronic renal failure, as well as in normal rats. The hormone or its analogue were administered intraperitoneally to vitamin-D-replete rats. Active Ca transport was increased in both spontaneously hypertensive rats (SHR) and in normotensive control WKY rats 5 h after calcitriol dosing of either 60 and 600 ng per rat. In WKY, calbindin-D9k content was slightly increased after the injection of 60 ng calcitriol, but not of 600 ng calcitriol whereas calbindin-D9k mRNA stayed essentially unchanged. In contrast, active Ca transport was significantly stimulated after the higher dose of 600 ng calcitriol. In SHR, while both doses of calcitriol increased active Ca transport, they had no stimulatory effect on calbindin-D9k mRNA or protein. In chronically uraemic rats, active Ca transport, duodenal calbindin-D9k and calbindin-D9k mRNA were stimulated after the injection of two subsequent doses of 300 ng calcitriol per rat. OCT treatment at same dosage led to a similar stimulation of calbindin-D9k and calbindin-D9k mRNA, but failed to induce an increase in active Ca transport. These results show that the stimulation of intestinal active Ca transport and calbindin-D9k can be entirely dissociated at the protein synthesis and the mRNA expression level (1) after calcitriol administration to normal and hypertensive rats, and (2) after OCT administration to uraemic rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Abnormal regulation of intestinal calbindin (CaBP9k) and calmodulin in the spontaneously hypertensive rat.

This review focuses particularly on abnormalities of Ca-binding proteins in transporting epithelia, which have been observed in various models of experimental hypertension. The enterocyte content of integral membrane Ca(2+)-binding protein (IMCAL) and calbindin-9k and the renal tubular calbindin-28k content have been shown to be decreased in the spontaneously hypertensive rat (SHR), compared with normotensive control rats (WKY). Similarly, calmodulin content was decreased in several tissues including the intestine; however, calmodulin activity was increased. In recent studies, the authors examined the response of intestinal calbindin-9k, calbindin-9k mRNA, and calmodulin contents to low-Ca and high-Ca diets in these two rat strains. It was shown that the SHR, unlike the WKY, was unable to augment intestinal calbindin-9k and calbindin-9k mRNA levels in response to a low-Ca diet of short duration. On the other hand, a high-Ca diet led to a similar decrease in calbindin-9k content in both SHR and WKY rats. Enterocyte calmodulin content was also diminished in the WKY, but not the SHR, fed such a high-Ca diet. Therefore, abnormal Ca-binding proteins could play a role in the disturbed Ca metabolism of arterial hypertension.

Animals↗