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Proneurotensin/neuromedin N (pro-NT/NN) is the common precursor of two biologically active related peptides, neuromedin N (NN) and neurotensin (NT). It undergoes a tissue-specific processing leading to the formation in some tissues and cancer cell lines of large peptides ending with the NT (large NT) or NN (large NN) sequence. In this study, we prepared and purified high amounts of recombinant large NT and large NN using the Drosophila S2 cell expression system. The binding and pharmacological properties of recombinant large peptides were characterized and compared to those of NT and NN using either COS cells transfected with the human subtype-1 NT receptor (hNTS1) or the human colon adenocarcinoma HT29 cell line that endogenously expresses hNTS1. Furthermore, the metabolic stability of the large peptides, when exposed to HT29 cells, was compared to that of NT and NN. Both large NT and large NN were able to bind to and activate hNTS1 with potencies that were approximately 10 times lower than that of their small counterpart. In addition, the large forms proved to be far less sensitive to degradation than the small peptides. Taken together, these data suggest that the large forms might represent endogenous, long-lasting activators of hNTS1 in a number of physiopathological situations.

Experiments were performed with human plasma irradiated in vitro or in vivo in order to evaluate the extent to which clastogenic factors might disturb the adaptive response to DNA-damaging factors currently studied in our laboratory. The studies were carried out with plasma isolated from whole blood given 4 Gy of X-rays in vitro and with plasma from people receiving local radiotherapy at a total dose of about 60 Gy gamma rays. Addition of irradiated plasma to culture medium did not result in a statistically significant increase in structural aberrations in chromosomes of non-irradiated normal blood.

The hydrogeochemistry of a small portion of a calcareous alluvial aquifer recharged by the Drac River (Grenoble, France) is characterized both in time and space. Significant changes in water chemistry are observed as the river water infiltrates into the aquifer. Processes occuring in the river bank (mostly biologically mediated) and in the aquifer (additional solid-liquid interactions) buffer some of the groundwater composition regardless of the variations in the river input. However, small zones (of enhanced biological activity due to low permeability and/ or high organic carbon content) located away from the river bank can induce significant localized changes in groundwater quality (such as locally high dissolved Mn due to the dissolutive reaction of MnO 2(s) and/or MnOOH (s) ).

Catecholamine metabolism was studied in vivo in the Cl adrenergic area of the rostral ventrolateral medulla oblongata in rats, using differential normal pulse voltammetry coupled with an activated carbon fiber microelectrode. Pharmacological evidence indicates that 3,4-dihydroxyphenylacetic acid, the major dopamine metabolite, is responsible for the electrochemical signal appearance in the C1 group, and that it reflects the Catecholamine synthesis rate, as previously reported in the locus coeruleus. Indeed, 3,4-dihydroxyphenylacetic acid was estimated to be formed from 77% of the intracellular dopamine, since its synthesis was increased by only 23%, after blockade of the dopamine-β-hydroxylase activity. Neuronal activation by retrograde electrical stimulation increased the electrochemical signal, as well as hemorrhage and hypotension, suggesting that the level of extracellular 3,4-dihydroxyphenylacetic acid is a good biochemical index of the C1 adrenergic cellular activity in baseline conditions and during cellular activation.

L'unite d'hebergement renforce (UHR), specifique des unites de soins de longue duree (USLD) est un lieu de vie et de soins qui fonctionne nuit et jour. Elle propose sur un meme lieu l'hebergement, les soins, les activites sociales et therapeutiques pour des personnes âgees repondant aux criteres d'admission en USLD et presentant des troubles du comportement perturbateurs severes dans le cadre de l'evolution d'une maladie d'Alzheimer ou de maladies apparentees.