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N Bernard

Publications and source records attributed to N Bernard.

144 records · Page 8Linked to original sources
PubMed1980

Modification of rat hemopexin properties upon heme binding.

Rat hemopexin and its complex with heme were found to have the same Stokes' radius, 3.9 nm, as determined by gel filtration. Therefore no polymerisation occurs as a result of heme binding. The conformational parameters calculated from circular dichroism spectra indicate that hemopexin and its complex consist of 20% beta sheet and mainly of disordered structure. No change of the secondary structure is therefore observed upon heme binding. Hemopexin reveals five bands by analytical electrofocusing with pI ranging from 5.5 to 5.95. This microheterogeneity is not due to sialic acid differences between the variants. Upon heme binding the pI of the variants decrease to lower values (from 4.8 to 5.25). This decrease in the pI value of hemopexin is thought to modify the tertiary structure through charge effects and may allow the binding of the heme-hemopexin complex to the hepatocytes.

Animals↗
PubMed1979

Pharmacokinetics and bioavailability of pyridinol carbamate in humans.

The pharmacokinetics of two pyridinol carbamate formulations were studied after a single oral administration in 10 healthy volunteers. An open one-compartment model described the evolution of plasma concentrations as a function of time. Pyridinol carbamate was rapidly absorbed (mean lag time from 0.36 to 0.38 hr). Its elimination half-life ranged from 3.3 to 7.9 hr. The two formulations were bioequivalent.

Adult↗
PubMed1975

[Isolation and physical chemical properties of rat hemopexin].

Rat hemopexin was purified by a procedure involving three different steps : ammonium sulfate precipitation, rivanol precipitation and DEAE-cellulose chromatography with concave gradient of molarity. Purity of the preparation was checked by three different methods : analytical ultracentrifugation, immunoelectrophoresis and acrylamide gel electrophoresis. The principal physical properties were studied. The amino acid and carbohydrate composition was determined and compared with that of human and rabbit hemopexin.

Amino Acids↗
PubMedDate not supplied

Personal exposure to nitrogen dioxide pollution and effect on plasma antioxidants.

We conducted a cross-sectional epidemiological study to evaluate personal exposure to nitrogen dioxide and its effect on blood antioxidants. Personal exposure of 107 volunteers was assessed for 14 d with passive monitors. We excluded heavy smokers (> 10 cigarettes/d) from the study. Sociodemographic and environmental data, as well as beta-carotene intake, were recorded. We mainly attributed the mean nitrogen dioxide personal exposure (31.9 +/- 12.7 microg/m3 [0.017 ppm or 0.70 microM/m3]) (R2 = 0.75) to residence site in the city, time spent in urban traffic, and use of gas stoves. The correlation between nitrogen dioxide exposure and blood antioxidant concentration was weak; in addition, the correlation coefficients for men and women were inconsistent. Nonetheless, we found some evidence of an interaction between carotene intake and nitrogen dioxide exposure: a significantly lower plasma beta-carotene level was evident among subjects who consumed < or = 4.5 mg/jour of carotene and who were exposed to nitrogen dioxide levels that exceeded 40 microg/m3 (0.021 ppm or 0.87 microM/m3) of nitrogen dioxide.

Adult↗
PubMedDate not supplied

Ozone exposure and blood antioxidants: a study in a periurban area in Southern France.

Major carotenoids in plasma--especially beta-carotene--are affected by oxidative stress (e.g., tobacco smoking). Environmental ozone induced oxidative stress in experimental in vitro and in vivo studies, and it also increased the incidence of lung cancer in mice. We proposed to measure, after controlling for other determinants, the impact of personal ozone exposure on carotenoids levels in plasma. During the summer, we recruited 58 volunteer subjects who worked in a periurban zone. We asked each subject to wear a passive sample, which measured ozone exposure for 5 consecutive d. At the end of this period, we assessed plasma antioxidants. We observed a negative significant regression coefficient between alpha- or beta-carotene and ozone exposure (r = -.39, p < .01, and r = -.45, p = .02, respectively). In a subsample of 45 nonsmoker subjects, among whom carotene intake was lower than the median intake value (i.e., 6.6 mg/d) of the overall group, we noted that a relatively low exposure to ozone (> or = 50 microg/m3 x h or > or = 23.8 ppb) induced a significant decrease in plasma beta-carotene levels (i.e., 0.7 micromol/l to 0.4 micromol/l). This significant decrease suggested that a high dietary intake of fruit or vegetables can have a beneficial influence on the levels of plasma antioxidants generated in response to ozone exposure.

Adult↗
PubMedDate not supplied

Cytochrome P-450-dependent arachidonate metabolites and renal functions in the Lyon hypertensive rat.

1. The present work aimed to assess the role of cytochrome P-450 (CP-450) metabolites of arachidonic acid such as epoxy-eicosatrienoic (EET) and hydroxyeicosatetraenoic acids (HETE) in the renal vasoconstriction and decreased natriuresis exhibited by genetically hypertensive (LH) rats of the Lyon strain. 2. The experiment was performed on single-pass isolated perfused kidney preparations from 8-week-old male LH rats and their low blood pressure (LL) controls. The effects of miconazole (an inhibitor of the formation of EET) and of 17-octadecynoic acid (17-ODYA, an inhibitor of both EET and HETE synthesis) were studied before and after stimulation of the kidneys with two noradrenaline (NA) infusions (65 and 110 nmol/L). 3. Unstimulated LH kidneys (n = 12) differed from LL (n = 12) by increased vascular resistance (RVR) and decreased glomerular filtration rate and urinary sodium excretion (UNaV). 4. Miconazole (1 mumol/L) did not change the functions of LH and LL unstimulated kidneys, but blunted the vasoconstrictor response to NA (110 nmol/L), the difference being significant in LH kidneys only (1.7 +/- 0.2 vs 3.6 +/- 1.2 mmHg/mL per min per g; P < 0.05). 5. Addition of 17-ODYA (3 mumol/L) to miconazole did not modify RVR in LH and LL kidneys or the response to NA infusion. On the contrary, it increased UNaV, the differences being significant in LH kidneys only (22.9 +/- 1.4 vs 17.5 +/- 1.4 mumol/min per g; P < 0.05 after NA 110 nmol/L). 6. It is suggested that EET may contribute to the elevated RVR and HETE to the reduced ability to excrete sodium, of LH kidneys.

Animals↗
PubMedDate not supplied

Nebulized cyclosporine for prevention of acute pulmonary allograft rejection in the rat: pharmacokinetic and histologic study.

BACKGROUND: With regard to limiting the systemic effects of cyclosporine A and obtaining better control of acute pulmonary allograft rejection, local immunosuppressive therapy with aerosolized cyclosporine A seems of interest. Given the in situ immunologic mechanisms of acute rejection, as well as the anatomic structure of the lung, this therapy is feasible as previously described by others. The aim of our study is to determine the pharmacokinetic parameters of nebulized cyclosporine A and the best modalities of administration. METHODS: In a pharmacokinetic study, the cyclosporine A was given either by intramuscular injection (10 mg/kg) or by aerosol at 10 and 25 mg/kg doses; 70 rats were killed at 25 and 50 minutes and 2, 4, 6, 8, 12, 24, or 48 hours after cyclosporine A administration. Cyclosporine A levels were measured in whole blood and in the lung. The areas under the concentration time curves were determined. Twenty-four lung transplantations were then performed. The rats were killed on postoperative day 9. Acute rejection was scored on a scale of 0 to 4, and cyclosporine A trough levels were measured in the lung and in the blood. RESULTS: With a jet nebulizer, the mass median aerodynamic diameter was 2.5 microns, with a standard geometric deviation of 2.3. In blood, the area under the concentration curve was greater for intramuscular (80.6 ng.hr/ml) than for aerosol administrations at 10 (15.1 ng.hr/ml) and 25 mg/kg (41.0 ng.hr/ml) doses. In the lungs, the area under the concentration curve was greater for the aerosol route at 25 mg/kg doses (588 ng.hr/mg) than for the low-dose (200 ng.hr/mg) or intramuscular administration (200 ng.hr/mg). The lung targeting index of cyclosporine A (ratio area under the concentration curve-lungs/area under the concentration curve-blood) was greater for both aerosol administrations than for the intramuscular route. In the study of the prevention of acute rejection, rats without immunosuppression (n = 6), rats receiving daily doses of cyclosporine A intramuscularly (10 mg/kg), and rats with aerosolized cyclosporine A daily (10 and 25 mg/kg/day) showed mean grades of acute rejection of, respectively, 4, 2.03 +/- 0.27, 2.33 +/- 0.52, and 2.17 +/- 0.46. The deposition of nebulized cyclosporine A was lower in transplanted than in native lung. CONCLUSIONS: Nebulized cyclosporine A allows better pulmonary concentration than intramuscular administration, and results in lower systemic levels. Prevention of acute rejection is as good with aerosolized cyclosporine A as with intramuscular cyclosporine A. This first pharmacokinetic study of nebulized cyclosporine A could lead to clinical applications.

Administration, Inhalation↗