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Biomedical subjects

N Henry

Publications and source records attributed to N Henry.

At least 19 recordsLinked to original sources

Pancreatitis in human immunodeficiency virus-infected children receiving dideoxyinosine.

To define predictive or contributory risk factors for pancreatitis in human immunodeficiency virus-infected children receiving dideoxyinosine (ddI), the authors evaluated 95 children, 3 months to 18 years of age, who had received ddI at 60 to 540 mg/m2 per day for a mean of 56 weeks. Pancreatitis developed in 7 patients (7%) but resolved in all upon withdrawal of ddI. Neither age, sex, nor CD4 count at study entry was predictive of pancreatitis, but pancreatitis appeared more likely to develop in hemophiliacs than in other patients (4 of 23 vs 3 of 72). Pancreatitis developed only in patients who received ddI at the highest dose levels (7 of 60 patients who received ddI at a dose > or = 360 mg/m2 per day vs 0 of 35 patients who received < or = 270 mg/m2 per day). Patients in whom pancreatitis developed had received a higher mean daily dose of ddI than patients with normal amylase and lipase levels throughout the study (348 mg/m2 vs 282 mg/m2), but no relationship with the cumulative dose or the duration of ddI therapy was observed. Although a statistically significant relationship between ddI plasma concentration (area under the curve) and pancreatitis was not conclusively demonstrated, as the number of patients in whom pancreatitis actually developed was small, such a relationship may have been obscured.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent

Ciprofloxacin therapy of experimental endocarditis caused by methicillin-susceptible or methicillin-resistant Staphylococcus aureus.

Ciprofloxacin was more effective (P less than 0.01) than either imipenem or nafcillin therapy of experimental methicillin-susceptible Staphylococcus aureus endocarditis in rabbits after 2 or 3 days of treatment. There was no significant difference between results of treatment of methicillin-susceptible S. aureus experimental endocarditis with ciprofloxacin and results with the combination of nafcillin and gentamicin. Ciprofloxacin was more effective (P less than 0.01) than vancomycin therapy of experimental methicillin-resistant S. aureus endocarditis after 3 days of treatment. After 5 days of treatment, there was no significant difference between the results of treatment of experimental methicillin-resistant S. aureus endocarditis with ciprofloxacin and results with vancomycin.

Animals

Synergistic incorporation of daunorubicin in erythrocytes in the presence of polyene antibiotics. Role of the membrane potential.

The synergistic incorporation into red blood cells of the antitumor compound daunorubicin, in the presence of the polyene antibiotics amphotericin B and vacidin A, depended on the composition of the external medium. Synergism was observed only for concentrations of polyene antibiotics that induce cation permeability. The same synergistic effect was observed with the K+ selective carrier, valinomycin, but this had a different dependence on the external medium composition. By using the membrane probe 3,3'-dipropylthiadicarbocyanine (diS-C3-(5], the synergistic effect was shown to occur under conditions where addition of the ionophores leads to hyperpolarization of the membrane.

Amphotericin B

Interaction of adriamycin with negatively charged model membranes: evidence of two types of binding sites.

The interaction of the antitumor compound adriamycin with negatively charged unilamellar phospholipid vesicles was studied. The negative charges were provided by cardiolipin or phosphatidic acid. By analyzing the changes in the circular dichroism spectrum of adriamycin, we demonstrated the presence of two different spectral patterns corresponding to two different binding sites (I and II) on the vesicles. In site I, the amino sugar of adriamycin is bound to the ionized phosphate of either cardiolipin or phosphatidic acid, and the dihydroxyanthraquinone lies outside the bilayer. In site II, the amino sugar is still bound to the phosphate, but the dihydroxyanthraquinone moiety is embedded in the bilayer. This has been shown by measuring spectroscopically the binding of the aglycon part to an external probe and by measuring the susceptibility of bound adriamycin to reduction by NADH dehydrogenase.

Cardiolipins

Co-operation between metastatic tumor cells and macrophages in the degradation of basement membrane (type IV) collagen.

The co-culture of mouse peritoneal macrophages and Lewis lung carcinoma cells induces the release of a metal-dependent type IV collagen-degrading proteinase which is not produced in detectable amounts by either cell type cultivated alone. Conditioned media of the co-cultures degrade both pepsin-extracted type IV collagen from human placenta and mouse type IV procollagen. Thus macrophages can interact with tumor cells to degrade basement membrane type IV collagen: this might be of importance to allow cancer invasion and metastasis.

Animals

[Experimental reproduction of lactic acidosis in the pony].

One pony has been subjected to the intravenous injections of L-lactic acid. Two other ponies have been trained to intracaecal administration of L-lactic acid or sucrose. The obtained results show that: Intravenous injection of lactic acid increases the concentration of histamin and lactic acid, decreases the level of magnesium and reduces the pressure of carbon dioxide in the blood (the control animals and the treated animals) without the clinical symptoms of lactic acidosis. Intracaecal administration of lactic acid induces a high liberation of histamin in the caecum (the control animals and the treated animals), however, the level of histamin in the blood is not modified. Intracaecal administration of sucrose decreases pH and increases the concentration of lactic acid in the caecum, although, in this case, the accumulation of histamin in the caecum appears only in the non-fasting ponies, the starved animals, and the fed animals, which suggests the necessity of food's proteins for histamin synthesis.

Acidosis

Collagen degradation by metastatic variants of Lewis lung carcinoma: cooperation between tumor cells and macrophages.

Interactions between cancer cells and host macrophages might have important regulatory roles in controlling the expression of the metastatic phenotype, particularly by regulating the production of proteases necessary for tissue invasion. To investigate that possibility, mouse macrophages and Lewis lung carcinoma (LLC) cells from four clonal subpopulations with either low or high metastatic ability were cultured on [14C]collagen (type l)-coated plates. They did not degrade collagen when they were cultured independently on that substrate, but they were induced to do so when macrophages and cancer cells were cultured together. An increased production of neutral collagenase and other neutral protease activities was observed simultaneously. The degree of stimulation of collagen degradation varied according to the cancer cell subpopulation present in the cocultures. For a given LLC cell subpopulation, similar degrees of stimulation of collagen degradation were achieved with either bone marrow-derived or resident peritoneal macrophages, either syngeneic (from C57BL/6 mice) or allogeneic; lower stimulations were obtained with thioglycolate-elicited peritoneal macrophages. Macrophage-conditioned culture media could be substituted for living macrophages to stimulate collagen degradation or collagenase secretion by LLC cells, but LLC cell-conditioned media did not stimulate collagen degradation by macrophages. This suggests that, in the cocultures, collagen degradation is achieved mainly by the cancer cells, not by the macrophages, and that it is induced by a soluble factor, a monokine, produced by the macrophages. That factor might be identical to a recently identified rabbit monokine that stimulates fibroblasts or synovial cells to degrade collagen and proteoglycan and to activate plasminogen, because rabbit macrophage-conditioned media containing that monokine also stimulated collagen degradation by LLC cells.

Animals

Metastatic heterogeneity of cells from Lewis lung carcinoma.

To allow investigations of the role of tumor cell proteases in invasion and metastasis, an attempt was made to obtain well-defined homogeneous populations of Lewis Lung carcinoma cells differing widely in their metastatic potential. From a single Lewis lung carcinoma, a parental line of cells was established and subsequently cloned so as to provide 18 clonal tumor cell lines. These clones differed in their ability to produce spontaneous, macroscopically visible metastases in the lung after i.m. inoculation into syngeneic C57BL/6 mice. Several of them were less metastatic than the parental line. The parental line expressed a metastatic behavior close to that of the high-metastatic cell subpopulations that it contained. There was, within certain limits, a good correlation between the potential for spontaneous lung metastases arising from a primary tumor and that for "artificial" lung colonies obtained after i.v. injection of the Lewis lung carcinoma cells. Although positively correlated with the growth rate of the tumor cells, the metastatic ability of the clones could not be considered as a mere reflection of the proliferation rates of the cells constituting the primary tumors. Differences in metastatic behavior observed among clones persisted in several cases after the cells had been maintained in culture for prolonged periods. However, this stability of the clones in vitro was not absolute. Indeed, some subclones isolated from the low-metastatic clone H122 displayed metastatic abilities which were lower than that of the parent clone. Furthermore, a significant increase in metastatic potential was once observed after a prolonged culture period of that same clone, H122. Thus, new metastatic phenotypes can emerged under in vitro culture conditions. However, the relative rarity of this event suggests that some metastatic heterogeneity already preexisted in vivo among the tumor cells.

Animals

Specific antibody-dependent binding of complement component C1q to hapten-sensitized lipid vesicles.

The binding of a component of human complement (C1q) to membrane-bound specific anti-nitroxide antibodies was studied as a function of the physical properties (fluid vs. solid) of vesicle lipids. The antibodies were bound to spin-label lipid haptens in the vesicle membrane. The binding of C1q to the sensitized vesicles shows a maximum as a function of specific IgG concentration. The binding of antibodies and of C1q to the vesicle membrane does not depend strongly on the physical state of the membrane lipids. even at low hapten (0.05 mol%) concentrations. These results are of significance for the understanding of the previously reported effect of lipid physical states on complement depletion.

Antibodies

Visualization of specific antibody and C1q binding to hapten-sensitized lipid vesicles.

Specific IgG antibodies directed against the spin-label nitroxide group present as a lipid hapten in single-compartment lipid vesicles have been visualized by using freeze-etch electron microscopy. Individual "particles" with diameters of the order of 20 nm are identified as single IgG molecules bound to lipid hapten. No significant aggregation of these IgG molecules was observed over a period of 1 hr in a dipalmitoyl phosphatidylcholine vesicle at 22 degrees. Binding of the human complement component C1q results in the formation of large (approximately 50-100 nm) asymmetric particles having a partially resolved substructure that may arise from individual IgG molecules bound to the membranes as well as to C1q. The binding of C1q appears to result in a clustering of membrane-bound IgG molecules. Samples containing a serum factor (perhaps anti-IgG antibodies) exhibit some IgG clustering distinct from that produced by Clq.

Complement C1

["Milk aflatoxin" and transfer of toxicity].

Diet including 20 p. 100 of lyophilised milk produced by Goat who consumes peanut meals containing 1,530, 79 and 54 microng/kg aflatoxins with 1,136, 64 and 54 microng/kg aflatoxin B1, is given to duckling during 23 days. There is no influence of this diet on growth, feed efficiency and liver or kidney histology. In contrast, direct consummation of Peanut meal, with the highest level of aflatoxins, produces 18 p. 100 mortality and characteristic injuries of aflatoxiocsis.

Aflatoxins

[Diet imbalances and aflatoxicosis].

Generally we know influences of diet's balances or imbalances upon toxicants. Some actions appear with aflatoxins as shown by studies on rat, pig, calf, poultry, turkey and duckling. According to species considered, oral administration of aflatoxins reduces food consummation, Nitrogen balance, respiratory coefficient. Therefore those modifications may be induced by a decrease of foodstuffs ingestion. It has been underlined that hypoproteic diet increases intoxication and diet rich in lipotropic factors decreases it. The greatest number of experiments carried out are concerning vitamins A and D. Authors are recounting their own experimentations upon relationships between Ducklings, aflatoxicosis, retinol consumption and cholecalciferol deficiency. In Duckling, diet deficient in vitamin D increases aflatoxins toxicity. Some relations exist with cytochrome P 450.

Aflatoxins

Pharmacodynamic study of a pyrophtalone: [methyl-2 (piperidino-2 ethyl-1)-1 dihydro 1-4 pyridylidene-4 yl]-2 indanedione 1-3. II. Mechanism of action.

The anti-inflammatory activity of the pyrophtalone derivative, [methyl-2 (piperidino-2 ethyl-1)-1 dihydro 1-4 pyridylidene-4 yl]-2 indanedione 1-3 or PpEtgammaL is not dependent upon adrenal gland stimulation. PpEtgammaL has an inhibitory effect neither on prostaglandin release after biosynthesis nor on prostaglandin synthetase. The reduced prostaglandin production, as result of drug action can be explained by impairment of substrate availability for this enzyme. There are several hypotheses, but according to the present results of our work, the most plausible one is an inhibition of unsaturated fatty acids release from cell membrane lipids.

Adipose Tissue

Pharmacodynamic study of a pyrophtalone: [methyl-2 (piperidino-2 ethyl-1)-1 dihydro 1-4 pyridylidene-4 yl]-2 indanedione 1-3. I. Anti-inflammatory activity.

The anti-inflammatory activity of a pyrophtalone [methyl-2 (piperidino-2 ethyl-1)-1 dihydro 1-4 pyridylidene-4 yl]-2 indanedione 1-3, has been demonstrated with different methods (carrageenan-induced edema of rat's paw, granuloma formation, adjuvant-induced arthritis). The anti-inflammatory potency is lower but sometimes comparable to that of phenylbutazone. Moreover, the acute toxicity and the ulcerogenic effect of the pyropthalone derivative are clearly less marked.

Animals