Neutron spin-echo study of sodium nitrite near the incommensurate transition.
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Biomedical subjects
Publications and source records attributed to D Durand.
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The effects of chronic ethanol intake were studied on the morphology of rat hippocampal granule cells. Sprague-Dawley rats were exposed to ethanol in a liquid diet for 5 months followed by a 3 week withdrawal period. A control group was fed similar amounts of the same diet but with ethanol replaced by maltose-dextrins. Intracellular recordings were performed using the hippocampal slice preparation and the granule cells from animals of both groups were injected with HRP. The ethanol treatment produced a significant increase in the average length of the dendrites of granule cells compared to the control group. Chronic ethanol intake produced a decrease in the number of dendrites in the proximal region of the tree (80-180 microns) but also a significant increase in the number of dendrites in the distal portion (260-340 microns). The decrease in the number of proximal dendrites suggests that ethanol could be affecting a population of neurons with afferent inputs in the proximal region of the tree or that ethanol could interfere with the normal maturation processes of the granule cells. The increase in the number of dendrites in the distal region of the tree suggests, however, an accelerated growth or sprouting of dendrites in the molecular layer.
The present study was aimed at determining the influence of nutrients supplied by a milk diet (glucose, amino acids, triglycerides) on hepatic somatomedin C (IGFi) production in vivo in four 30-d-old milk-fed calves fitted with chronically indwelling catheters in hepatic (HV), portal (PV) and mesenteric veins and in the hepatic artery (HA), and with electromagnetic flow-meters on HA and PV. Fasting for 16 h induced a decrease (P less than 0.01) in hepatic IGF1 production (nmol/kg body-weight (BW) for 6 h) (1.1 (SE 0.2) v. 6.6 (SE 0.7) in control animals). Infusion of glucose (1.8 g/kg BW for 4 h) or a mixture of amino acids (Azonutril; R. Bellon, Neuilly sur Seine; 62.5 mg nitrogen/kg BW for 3 h) in a mesenteric vein led to no significant effect on hepatic IGF1 production for 6 h (1.2 (SE 0.3) and 0.7 (SE 0.3) nmol/kg BW respectively) compared with fasted calves. Infusion of chylomicrons purified from milk-fed calves (10.5 mg/h per kg BW, i.e. 0.16 mg triglycerides/kg BW per min) enhanced significantly (P less than 0.01) the hepatic production of IGF1 (mean value for 6 h: 5.3 (SE 0.8) nmol/kg BW). Infusion of Intralipid (7 mg triglycerides/kg BW per min) induced a slight but significant hepatic IGF1 production which amounted to 3.5 (SE 0.4) nmol/kg BW (P less than 0.1 compared with chylomicron treatment) and it began only 5 h after starting the infusion. Neither triglyceride nor chylomicron infusion significantly modified hepatic blood flow. Thus, these results demonstrate for the first time the role of lipids in the regulation of hepatic IGF1 production in vivo.
In order to determine the central or peripheral origin of the starvation-induced modifications of growth hormone (GH) and thyroid-stimulating hormone (TSH) secretions, the effects of starvation were studied in freely moving male rats with hypothalamo-hypophyseal disconnection. Five days after the disconnection GH secretion exhibited lower maximal values and higher trough levels and ultradian pulsatile secretion was lost as compared to controls. TSH levels were also decreased. The lesion did not modify pituitary somatostatin (SRIF) receptors as assessed by 125I-Tyr-O-D-Trp-8-SRIF binding or inhibition of adenylate cyclase activity. On the other hand, the growth hormone releasing factor (GRF) capacity to stimulate adenylate cyclase was strongly reduced by the lesion without modification of the affinity. Exposure to 72 h food deprivation decreased GH pulses and TSH levels in control rats but did not modify GH secretory profiles or TSH levels of lesioned rats. Plasma glucose and insulin levels were equally decreased after fasting in control and lesioned rats. Altogether, our results demonstrate that starvation-induced modifications of GH and TSH secretions are of central origin while glucose and insulin changes are peripherally triggered. They suggest that the hypothalamus is the only source of SRIF implicated in this effect.
The objective was to clarify the possible role of meals in the nycthemeral evolution of cortisol and the influence of intestine absorption kinetic of nutrients. Preruminant calves were fed two kinds of diets, a conventional curdled milk and a milk that did not curdle in the abomasum. These calves were also fasted for 24 h. Blood was sampled regularly during a 24-h period under three different dietary situations. Daily mean plasma cortisol was lower in calves fed uncurdled milk than in those fed curdled milk or fasted. Diurnal changes in plasma cortisol were characterized in fed animals by sharp postprandial decreases; the morning meal induced a more intense decrease than the evening one, which was followed by a regular increase of cortisol concentrations overnight. Between meals, several peak values were detected at the same times in all animals with both kinds of meals. The postprandial decreases did not occur in fasted animals, and peak values could not be linked to those occurring when animals were fed. Thus, cortisol secretion by adrenals seemed to be influenced by nutrient intestinal absorption, whereas during fasting different mechanisms were involved.
SUMMARY The De La Visite project makes a contribution to a major social challenge : putting in place preventive measures with the long-term goal of diminishing abuse and negligence of children in the home. This project consisted of : 1) having nonprofes-sional workers visit at home new parents living in three economically disadvantaged neighbourhoods on the Island of Montreal ; 2) evaluating this new service via an innovative research method utilizing both an experimental instrument and a qualitative approach, in order to determine whether to propose implementation in the Montreal region. The first part of this article presents the project's premises and goals. The second part gives an overview of the experiment and discusses, for those who offer or wish to offer a similar service, what was learned from a detailed analysis of how the service worked. The third part of the article discusses the effects of the experiment.
In approximately 10 p. 100 of the cases stenosis of the renal artery cannot be satisfactorily dilated by percutaneous transluminal angioplasty (PTA), and about 10 p. 100 of the patients successfully dilated have short-term restenosis. The excellent results obtained experimentally and clinically with the implantation of percutaneous intravascular stents have prompted us to use this material in the renal arteries. Stents were implanted in 10 patients who were followed up for periods of 1 to 16 months. Eight of them had restenosis after PTA; five of these stenoses were due to atheroma, 2 to fibromuscular dysplasia and 1 to Takayasu's disease. Two patients were implanted from the start owing to the insufficient results of PTA. Seven patients had severe arterial hypertension most probably of renovascular origin. Three patients had hypertension associated with moderate renal failure. Implantation was performed after a previous PTA. Adjuvant treatments and monitoring were the same in every case with, in particular, radiological control examination after one and six months. The implantations themselves were uneventful, and immediate control showed almost perfect anatomical restoration in all patients. On subsequent controls, arterial patency was preserved in all but one case. All patients showed significant clinical improvement. These results are most encouraging. They suggest that intravascular stents constitute an interesting solution when PTA is insufficient in the treatment of renal artery stenosis.
Among others, ciclosporin had the advantage of decreasing appreciably the incidence of osteonecrosis after renal transplantation. However, the authors have isolated, in three renal transplant patients and one heart transplant patient, treated with ciclosporin, a new syndrome consisting of bilateral and symmetrical joint pain, affecting the lower extremities and lasting almost one year. Subsiding of the radiological aspect and the isotopic hyperfixation of the affected joints, at the end of the evolution, as well as the histological aspect of the bone surrounding the joints, remind somehow of algodystrophy. In both cases, the severity of the pain seemed to depend on the doses of ciclosporin, indicating that this molecule could play a role in the occurrence of this syndrome.
The in vivo role of the liver in lipoprotein homeostasis in the preruminant calf, a functional monogastric, has been evaluated. To this end, the hydrodynamic and physicochemical properties, density distribution, apolipoprotein content, and flow rates of the various lipoprotein particle species were determined in the hepatic afferent (portal vein and hepatic artery) and efferent (hepatic vein) vessels in fasting, 3-week-old male preruminant calves. Plasma lipoprotein profiles were established by physicochemical analyses of a series of subfractions isolated by isopycnic density gradient ultracentrifugation. Triglyceride-rich very low density lipoproteins (VLDL) (d less than 1.018 g/ml) were minor plasma constituents (approximately 1% or less of total d less than 1.180 g/ml lipoproteins). The major apolipoproteins of VLDL were apoB-like species, while the complement of minor components included bovine apoA-I and apoC-like peptides. Particles with diameters (193-207 A) typical of low density lipoproteins (LDL) were present over the density interval 1.026-1.076 g/ml; however, only LDL of d 1.026-1.046 g/ml were present as a unique and homogeneous size subspecies, containing the two apoB-like species as major protein components in addition to elevated cholesteryl ester contents. LDL represented approximately 10% of total d less than 1.180 g/ml lipoproteins in fasting plasma from all three hepatic vessels. Overlap in the density distribution of particles with the diameters of LDL and of high density lipoproteins (HDL) occurred in the density range from 1.046 to 1.076 g/ml; these HDL particles were 130-150 A in diameter. HDL were the major plasma particles (approximately 90% of total d less than 1.180 g/ml substances) and presented as two distinct populations which we have termed light (HDLL) and heavy (HDLH) HDL. Light HDL (d 1.060-1.091 g/ml) ranged in size from 120 to 140 A, and were distinguished by their high cholesteryl ester (29-33%) and low triglyceride (1-3%) contents; apoA-I was the principal apolipoprotein. Small amounts of apolipoproteins with Mr less than 60,000, including apoC-like peptides, were also present. Heavy HDL (d 1.091-1.180 g/ml) accounted for almost half (47%) of total calf HDL, and like HDLL, were also enriched in cholesteryl ester and apoA-I; they ranged in size from 93 to 120 A. The protein moiety of HDLH was distinct in its possession of an apoA-IV-like protein (Mr 42,000). Blood flow rates were determined by electromagnetic flowmetry, thereby permitting determination of net lipoprotein balance across the liver. VLDL were efficiently removed during passage through the liver (net uptake 1.06 mg/min per kg body weight).(ABSTRACT TRUNCATED AT 400 WORDS)
PGC counts were carried out on larvae of Pleurodeles waltl (urodele amphibia) issued from standard, monosexual male and monosexual female offspring while the genital ridges were settling. During this period, which is characterized by a zero mitotic index (and is therefore called the Po period), and which lasts from stage 35 to stage 41, no PGC proliferation occurs. A statistical analysis indicated that PGC counts per larva are sex genotype independent and that offspring may be divided into three groups with average PGC counts of 96.9, 51.0 and 31.1, respectively. A fourth group with an average of 18.3 PGCs has been identified using experimental larvae reared at 30 degrees C from stage 30. The PGC count of 96.9 would result from at least three mitotic cycles. Before the Po period, germ cells are not identifiable. A hypothesis concerning genetic control of PGC proliferation before Po was deduced from this analysis.
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Two cases of Goodpasture's syndrome with severe pulmonary haemorrhage and normal renal function are described. In spite of minor (patient 2) or even no (patient 1) biological or light microscopic signs of glomerulonephritis, immunofluorescence of immunoglobulin G (IgG) was strongly positive in a linear fashion along the glomerular basement membranes in both patients. We suggest that renal biopsy in patients with apparently idiopathic pulmonary haemorrhage may lead to an early diagnosis of Goodpasture's syndrome. It is not possible in this disease to recognize on presentation those patients who will remit spontaneously and those who will undergo severe disease. The deadly evolution for patient 1 and some cases in the literature lend support to the notion that cytostatics and plasma exchange must be added to corticosteroids, even if pulmonary haemorrhage is not active and renal function is normal at the time.
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To investigate whether the effects of testosterone (T) on endosteal bone metabolism may be mediated by growth hormone (GH), intact male mice were infused for ten days with T (5 or 15 mg/kg/d) alone, or combined either with native somatostatin (SRIF) (220 micrograms/kg/d) or with the long-acting somatostatin analog SMS 201-995. Testosterone infusion induced a dose-dependent increase in histomorphometric parameters of bone formation, causing a 25% increase in osteoblastic and osteoid surface and 10% to 12% stimulation of the matrix and mineral appositional rates. Stimulation of bone formation rate was associated with a 2- to 3-fold increase in the incidence of serum GH peaks of high amplitude. SRIF (220 micrograms/kg/d) and SMS at low dose (4.32 micrograms/kg/d) decreased parameters of bone formation by 20% to 25%. At a higher dosage (13 micrograms/kg/d), which mildly decreased serum glucose and longitudinal bone growth, SMS further reduced bone formation rate. Infusion of SRIF with T (5 mg/kg/d) blunted the stimulatory effect of T. Similarly, infusion of a high dose of SMS (13 micrograms/kg/d), together with T (15 mg/kg/d), abolished the effect of T (15 mg/kg/d) without altering serum glucose or mineral levels. The effect of SRIF on testosterone-induced (5 mg/kg/d) bone formation was associated with inhibition of T-induced high-amplitude GH peaks. The results indicate that T stimulates the osteoblastic bone formation in association with increased GH secretion, whereas SRIF and the analog SMS produce inhibitory effects.
The effects of growth hormone and insulin on the activity of pyruvate dehydrogenase were examined in the rat, both in vivo and in isolated hepatocytes. Liver mitochondria isolated from rats killed from five to 45 minutes after injection of 50 micrograms/100 g human growth hormone (hGH) or 25 micrograms/100 g insulin displayed a significant increase in the activity of basal pyruvate dehydrogenase (38% and 48% above control at ten minutes, respectively). These changes probably result from the conversion of the phosphorylated form to the nonphosphorylated form of pyruvate dehydrogenase since total enzyme activity was unaffected. Treatment of isolated hepatocytes by hGH or insulin also led to an increase in pyruvate dehydrogenase activity which was maximal (25% above control value) at 15 minutes. Later, activation progressively decreased and was no longer detectable at 60 minutes. The concentrations of hGH or insulin required for maximal activation were 100 nmol/L and 20 nmol/L, respectively, and the concentration required for half-maximal stimulation was 2 nmol/L for both hormones. The effects of 100 nmol/L hGH and 100 nmol/L insulin on pyruvate dehydrogenase activity were not additive. Basal pyruvate dehydrogenase activity in hepatocytes exhibited linear kinetics; hGH or insulin increased the Vmax of the enzyme without changing its Km and did not affect the Vmax of the total enzyme activity. It is concluded that growth hormone is as potent and as efficient as insulin in its ability to stimulate the activity of liver pyruvate dehydrogenase, and thus may be a physiological activator of this enzyme.
Platelet alpha 2- and leucocyte beta 2-adrenoceptors (as well as noradrenaline and adrenaline plasma levels) were studied in five patients with confirmed phaeochromocytoma using tritiated yohimbine and iodated cyanopindolol, respectively, before and after tumour removal. Patients with phaeochromocytoma had a lower leucocyte iodated cyanopindolol binding than control subjects, but no change in platelet tritiated yohimbine binding. Plasma catecholamine levels were higher than controls. Tumour removal induced a return to normal values of leucocyte iodated cyanopindolol binding and a decrease in plasma catecholamine levels. These results underline the potential interest of leucocyte beta-adrenoceptor quantification in the diagnosis and the follow-up of phaeochromocytoma. Pharmacologically, they show that down-regulation occurs in vivo for leucocyte beta 2-adrenoceptors but not for platelet alpha 2-adrenoceptors.
Preruminant calves bearing indwelling catheters in the hepatic artery, the portal and the hepatic veins were fed with two kinds of diets, a conventional curdled milk diet and a milk diet which was uncurdled in the abomasum. Measurements of plasma cortisol in blood sampled regularly during the 24 hr of the day indicated that with curdled milk, cortisol concentrations were significantly higher than with uncurdled milk. Nycthemeral changes were characterized by high values before meals and by postprandial decreases. Between meals, several peak values were observed and in the night a regular increase occurred. With both kinds of meals, cortisol evolutions were similar though peak values were higher with the curdled milk.