Tailoring the photoelectrochemistry of catalytic metal-insulator-semiconductor (MIS) photoanodes by a dissolution method.

Apart from being key structures of modern microelectronics, metal-insulator-semiconductor (MIS) junctions are highly promising electrodes for artificial leaves, i.e. photoelectrochemical cells that can convert sunlight into energy-rich fuels. Here, we demonstrate that homogeneous Si/SiOx/Ni MIS junctions, employed as photoanodes, can be functionalized with a redox-active species and simultaneously converted into high-photovoltage inhomogeneous MIS junctions by electrochemical dissolution. We also report on the considerable enhancement of performance towards urea oxidation, induced by this process. Finally, we demonstrate that both phenomena can be employed synergistically to design highly-efficient Si-based photoanodes. These findings open doors for the manufacturing of artificial leaves that can generate H2 under solar illumination using contaminated water.

Supported pulmonary surfactant bilayers on silica nanoparticles: formulation, stability and impact on lung epithelial cells.

Studies have shown that following exposure to particulate matter, ultrafine fractions (<100 nm) may deposit along the respiratory tract down to the alveolar region. To assess the effects of nanoparticles on the lungs, it is essential to address the question of their biophysicochemical interaction with the different pulmonary environments, including the lung lining fluids and the epithelia. Here we examine one of these interactive scenarios and study the role of supported lipid bilayers (SLB) in the effect of 40 nm fluorescent silica particles on living cells. We first study the particle phase behavior in the presence of Curosurf®, a pulmonary surfactant substitute used in replacement therapies. It is found that Curosurf® vesicles interact strongly with the nanoparticles, but do not spontaneously form SLBs. To achieve this goal, we use sonication to reshape the vesicular membranes and induce lipid fusion around the particles. Centrifugal sedimentation and electron microscopy are carried out to determine the optimum coating conditions and layer thickness. We then explore the impact of surfactant SLBs on the cytotoxic potential and interactions towards a malignant epithelial cell line. All in vitro assays indicate that SLBs mitigate the particle toxicity and internalization rates. In the cytoplasm, the particle localization is also strongly coating dependent. It is concluded that SLBs profoundly affect cellular interactions and functions in vitro and could represent an alternative strategy for particle coating. The current data also shed some light on the potential mechanisms pertaining to the particle or pathogen transport through the air-blood barrier.

[Safety management and compliance with rules]. / Management des risques et respect des règles.

The design of rules (laws, norms, policies, procedures, protocols) and the implementation of a management that aimed at conforming the behaviors of operators with these rules has long been the dominant approach to improve safety in socio-technical systems. This approach has proven to be effective in enhancing safety by enabling organizations to cope with predictable risks and failures. However, in our modern and constantly evolving socio-technical systems, where the management of unforeseen situation has become the rule, this approach has shown its limitations: operators' initiatives, which sometimes deviate from rules, are equally important for maintaining safety. Therefore, while the rules remain a key feature of risk management, the challenge is not the search for total compliance with rules, but the permanent monitoring of their use to detect and distinguish gaps that constitute a drift towards the accident from gaps that highlight that the rule has become inappropriate and which the compliance with may prove dangerous for safety.

Fabric Softener-Cellulose Nanocrystal Interaction: A Model for Assessing Surfactant Deposition on Cotton.

There is currently a renewed interest for improving household and personal-care formulations to provide more environment-friendly products. Fabric conditioners used as softeners have to fulfill a number of stability and biodegradability requirements. They should also display significant adsorption on cotton under the conditions of use. The quantification of surfactant adsorption remains however difficult because the fabric-woven structure is complex and deposited amounts are generally small. Here, we propose a method to evaluate cellulose-surfactant interactions with increased detection sensitivity. The method is based on the use of cellulose nanocrystals (CNCs) in lieu of micron-sized fibers or yarns, combined with different techniques, including light scattering, optical and electron microscopy, and electrophoretic mobility. CNCs are rod-shaped nanoparticles in the form of 200 nm laths that are negatively charged and can be dispersed in bulk solutions. In this work, we use a double-tailed cationic surfactant present in fabric softener. Results show that the surfactants self-assemble into unilamellar, multivesicular, and multilamellar vesicles, and the interaction with CNCs is driven by electrostatics. Mutual interactions are strong and lead to the formation of large-scale aggregates, where the vesicles remain intact at the cellulose surface. The technique developed here could be exploited to rapidly assess the fabric conditioner efficiency obtained by varying the nature and content of their chemical additives.

Efficient routes towards a series of 5,5'-bithiazolidinylidenes as π-electron acceptors.

Different approaches have been studied in order to prepare efficiently the sulfur rich electron acceptor, DEBTTT. Among the various routes used, the one going through the synthesis of a bicyclic derivative, where the thiazole-2-chalcogenone is fused with a 1,3-dithiole-2-one, leads to the target molecule under milder conditions and better yield. Thus, this approach has been explored for the synthesis of a series of acceptors either by modifying the substituent on the thiazole core or by changing the exocyclic chalcogen atoms. All these sulfur rich electron acceptors exhibit short intra- and intermolecular SS contacts in the solid state. Electrochemical investigations show that the nature of the exocyclic chalcogen atom of the thiazole ring has a significant influence on the accepting ability as a cathodic shift of about 220 mV is observed just by changing sulfur for oxygen. This structural modification enables the tuning of the redox properties.

[Treatment specifics for spontaneous pneumothorax in flight personnel]. / Spécificités de la prise en charge du pneumothorax spontané chez le personnel navigant.

Spontaneous pneumothorax is one cause of aeronautical unfitness in flight personnel, because of the risk of recurrence in flight, making it an issue of flight safety. Specific treatment is required for fighter pilots, pilots flying single-pilot and pilots in professional training: surgical synthesis via video-thoracoscopy is obligatory from the first episode. Considering the exposure to an accumulation of aeronautical factors that are likely to encourage pneumothorax recurrence in flight, it is apical pleurectomy together with abrasion of the remaining pleura and resection of bullae/blebs that is required for fighter pilots to allow them to recover aeronautical fitness unrestrictedly. For all other categories of flight personnel, treatment is no different from that of the common patient. Knowledge of these treatment specifics is essential, to avoid unnecessary systematic surgical indication for all flight personnel, or jeopardise professional fitness in some of them due to inappropriate treatment.

[Role of endovascular treatment of symptomatic splanchnic artery stenoses in HIV patients: report of three cases]. / Place du traitement endovasculaire des sténoses symptomatiques d'artères digestives chez les sujets infectés par le VIH: trois cas.

Patients with HIV or AIDS frequently present with GI symptoms, sometimes due to early and diffuse atherosclerosis. We report 3 cases of HIV patients with abdominal pain due to severe splanchnic arterial stenosis. Only one patient presented typical clinical findings of mesenteric ischemic. Endovascular treatment was performed in all three cases. Good clinical outcome was immediate in 2 cases. In the third case, subsequent bowel resection was required due to irreversible ischemic injury in spite of local thrombolysis and endovascular revascularization in a patient presenting with acute severe mesenteric ischemia. In all three cases, vascular patency was demonstrated at follow-up. Mesenteric ischemia is a severe complication requiring early diagnosis in HIV patients, especially those with vascular risk factors, especially since endovascular treatment is a valid therapeutic option.

Stable oxide nanoparticle clusters obtained by complexation.

We report on the electrostatic complexation between polyelectrolyte-neutral copolymers and oppositely charged 6-nm crystalline nanoparticles. For two different dispersions of oxide nanoparticles, the electrostatic complexation gives rise to the formation of stable nanoparticle clusters in the range 20-100 nm. It is found that inside the clusters, the particles are "pasted" together by the polyelectrolyte blocks adsorbed on their surface. Cryo-transmission electronic microscopy allows visualization of the clusters and determination of the probability distribution functions in size and in aggregation number. The comparison between light scattering and cryo-microscopy results suggests the existence of a polymer brush around the clusters.

Role of protein kinases in the prolactin-induced intracellular calcium rise in Chinese hamster ovary cells expressing the prolactin receptor.

There is still only limited understanding of the early steps of prolactin signal transduction in target cells. It has been shown that prolactin actions are associated with cell protein phosphorylation, Ca2+ increases, and so on. However, the link between the activation of kinases and calcium influx or intracellular Ca2+ mobilization has not yet been clearly established. Chinese hamster ovary (CHO) cells, stably transfected with the long form of rabbit mammary gland prolactin receptor (PRL-R) cDNA were used for PRL-R signal transduction studies. Spectrofluorimetric techniques were used to measure intracellular calcium ([Ca2+]i) in cell populations with Indo1 as a calcium fluorescent probe. We demonstrate that, although protein kinase C activation (PMA or DiC8) caused a calcium influx in CHO cells, prolactin-induced PKC activation was not responsible for the early effect of prolactin on [Ca2+]i. Activation of protein kinase A (PKA) or protein kinase G did not modify [Ca2+]i and inhibition of PKA pathway did not affect the prolactin response. In the same way, phosphatidylinositol-3 kinaseinhibition had no effect on the prolactin-induced Ca2+ increase. On the other hand, tyrosine kinase inhibitors (herbimycin A, lavendustin A, and genistein) completely blocked the effect of prolactin on [Ca2+]i (influx and release). W7, a calmodulin-antagonist, and a specific inhibitor of calmodulin kinases (KN-62), only blocked prolactin-induced Ca2+ influx but had no significant effect on Ca2+ release. Using pharmacological agents, we present new data concerning the involvement of protein phosphorylations in the early effects of prolactin on ionic channels in CHO cells expressing the long form of PRL-R. Our results suggest that, at least in the very early steps of prolactin signal transduction, serine-threonine phosphorylation does not participate in the prolactin-induced calcium increase. On the other hand, tyrosine phosphorylation is a crucial, very early step, since it controls K+ channel activation, calcium influx, and intracellular calcium mobilization. Calmodulin acts later, since its inhibition only blocks the prolactin-induced Ca2+ influx.

Distinct cytoplasmic regions of the prolactin receptor are required for prolactin-induced calcium entry.

Two cytoplasmic regions of the prolactin (PRL) receptor are well documented for their participation in PRL signal transduction, the membrane proximal box 1 and the COOH-terminal region. In order to study the role of these regions in PRL-induced Ca2+ increase, we use Chinese hamster ovary (CHO) cells stably transfected with mutated PRL receptor cDNA. These cells express the long form of PRL receptor deleted from box 1 (CHO Delta1 cells) or the 141 amino acids of the COOH-terminal region (CHO H3 cells). The patch-clamp technique in "whole-cell" configuration and microfluorimetric techniques were used singly or in combination. Data obtained for these cells were compared with those we have recently published using CHO cells expressing the wild-type long form of the PRL receptor (CHO TSE32). In contrast to CHO TSE32 cells, exposure of CHO Delta1 or H3 cells to PRL (0.05-50 nM) did not modify [Ca2+]i. We have previously shown that the PRL-induced calcium influx via voltage-insensitive, Ca2+ channels was due to the activation of tyrosine kinase-dependent K+ channels that hyperpolarize the CHO TSE32 cell membrane (hyperpolarization-driven Ca2+ influx). Therefore, two events are involved in PRL-induced Ca2+ changes (i) JAK2-activation of K+ channels and (ii) intracellular messenger-opening of Ca2+ channels. In CHO Delta1 cells, PRL (0.05-50 nM) neither hyperpolarized the membrane potential nor stimulated the JAK2-dependent K+ current, confirming the pivotal role played by box 1/JAK2 in the PRL-induced activation of K+ channels. However, when these cells were voltage-clamped below the resting membrane potential, application of 5 nM PRL resulted in an increase in Ca2+ influx. Therefore, box 1/JAK2 was not involved in the opening of these Ca2+ channels. In CHO H3 cells, 5 nM PRL activated the K+ current and hyperpolarized the membrane potential without any effect on [Ca2+]i. Moreover, PRL was also ineffective on CHO H3 cells voltage-clamped below the resting membrane potential. Therefore, the COOH-terminal region is involved in the production of the intracellular messenger that opens voltage-independent Ca2+ channels. We conclude from these findings that box 1 and COOH-terminal regions are both needed for PRL-induced Ca2+ changes.

Tubocurarine blocks a calcium-dependent potassium current in rat tumoral pituitary cells.

We investigated the effects of potassium channel inhibitors on electrical activity, membrane ionic currents, intracellular calcium concentration ([Ca2+]i) and hormone release in GH3/B6 cells (a line of pituitary origin). Patch-clamp recordings show a two-component after hyperpolarization (AHP) following each action potential (current clamp) or a two-component tail current (voltage-clamp). Both components can be blocked by inhibiting Ca2+ influx. Application of D-tubocurarine (dTc) (20-500 microM) reversibly suppressed the slowly decaying Ca2+-activated K+ tail current (I AHPs) in a concentration-dependent manner. On the other hand, low doses of tetraethylammonium ions (TEA+) only blocked the rapidly decaying voltage- and Ca2+-activated K+ tail current (I AHPf). Therefore, GH3/B6 cells exhibit at least two quite distinct Ca2+-dependent K+ currents, which differ in size, voltage- and Ca2+-sensitivity, kinetics and pharmacology. These two currents also play quite separate roles in shaping the action potential. d-tubocurarine increased spontaneous Ca2+ action potential firing, whereas TEA increased action potential duration. Thus, both agents stimulated Ca2+ entry. I AHPs is activated by a transient increase in [Ca2+]i such as a thyrotrophin releasing hormone-induced Ca2+ mobilization. All the K+ channel inhibitors we tested: TEA, apamin, dTC and charybdotoxin, stimulated prolactin and growth hormone release in GH3/B6 cells. Our results show that I AHPs is a good sensor for subplasmalemmal Ca2+ and that dTc is a good pharmacological tool for studying this current.

Dual Effect of Prolactin on Protein Kinase C Activity in CHO Cells Expressing Functional Prolactin Receptors.

We investigated the effects of prolactin (PRL) on the protein kinase C (PKC) activity in Chinese hamster ovary (CHO-E32) cells stably transfected with rabbit mammary gland PRL receptor cDNA. These cells express a functional long form of PRL-R. A 10-min to 2-hour treatment with 5 nM PRL resulted in the translocation of PKC activity from the cytosol to the membrane. Longer treatment (10-24 h) with the same concentration of PRL decreased the PKC activity in both particulate and cytoplasmic fractions. The PRL effect was dose dependent: maximal action was obtained with 1-10 nM. The PRL-induced activation of PKC was blocked by 20 nM staurosporine, a PKC inhibitor. Two inhibitors of tyrosine kinase, herbimycin A (1.75 &mgr;M) and genistein (100 &mgr;M), had no effect on PRL-induced activation of PKC. Copyright 1996 S. Karger AG, Basel

The Lipidosterolic Extract fromSerenoa repens Interferes with Prolactin Receptor Signal Transduction.

The lipidosterolic extract from the saw palmetto Serenoa repens (LSESr) is commonly used for medical treatment of benign prostatic hypertrophia due to its ability to inhibit 5alpha-reductase which permits the conversion of testosterone to dihydrotestosterone, the active androgen on prostate cell proliferation. However, the complete action mechanism of LSESr is still unknown. Several lines of evidence suggest that, in addition to inhibition of 5alpha-reductase, it may interfere with the action of prolactin (PRL). We therefore investigated a possible interference of this plant extract with another hormone that controls prostate gland growth, PRL. As the action mechanism of PRL is now fully documented in Chinese hamster ovary cells expressing the PRL receptor, we have conducted our experiments on these cells. In this study, using electrophysiological (whole-cell recording and single-channel recording), microspectrofluorimetric and biochemical techniques, we show that LSESr (1-30 &mgr;g/ml) reduced the basal activity of a K(+) channel and of protein kinase C (PKC) in CHO cells. In addition, pretreatment of the cells with 1-10 &mgr;g/ml LSESr for 6-36 h abolished the effects of PRL on [Ca(2+)](i), K(+) conductance and PKC. LSESr may block PRL-induced prostate growth by inhibiting several steps of PRL receptor signal transduction. LSESr may also be useful for diseases implicating PRL. Copyright 1995 S. Karger AG, Basel

Prolactin and growth hormone release and calcium influx are stimulated by galanin within a 'window' range of concentrations in pituitary GH3 B6 cells.

Galanin is widely distributed throughout the rat neural and endocrine system with the highest concentration in the anterior pituitary. The effects of galanin were investigated in rat tumor pituitary cells (GH3/B6). A single stimulation with galanin caused prolactin (PRL) and growth hormone (GH) release within a narrow range of concentrations (10(-11)-10(-9) M). However, secretory responses were not consistently observed upon subsequent galanin stimulation. Galanin triggered a rise in cytosolic Ca2+ (burst in [Ca2+]i transients) with a similar responsiveness. By contrast, no change in PRL mRNA was detectable in response to the peptide. These data suggest that galanin which binds to high-affinity receptors in anterior pituitary cells can exert subtle modulations of pituitary cell functions.

[Long-term induced effects by only one treatment with ketoconazole on rat tumoral pituitary cells (GH3/B6 strains)]. / Effets induits à long terme par un seul traitement de kétoconazole sur des cellules tumorales hypophysaires de rat (lignée GH3/B6).

Ketoconazole, an imidazole is a powerful antimycotic that has recently been used in the treatment of endocrinological and lipid metabolism disorders as well as in anti-cancer chemotherapy. When rat mammosomatotropic cells are treated for 30 hrs., this drug produces different effects depending on whether cells are normal or tumoral (GH3/B6). A dose of 10 microM had no effect in normal cells, however, in tumoral cells it had dramatic effects: (i) 50% of the cells are killed and those which survive no longer proliferate and they secrete GH but not PRL; (ii) they respond to GHRH in a dose-dependent manner, while normal cells do not under similar culture conditions; (iii) the lipid composition of the membrane is modified as indicated by the increase in arachidonic acid turn-over and the dramatic change in the distribution of its metabolites. For the moment we cannot explain these data.

Galanin evokes a cytosolic calcium bursting mode and hormone release in GH3/B6 pituitary cells.

The effects of galanin on secretion and cytosolic free Ca2+ concentration ([Ca2+]i) have been studied in GH3/B6 pituitary cells. Prolactin (PRL) and growth hormone (GH) release was measured in column perifusion experiments; [Ca2+]i was monitored in single cells by dual emission microspectrofluorimetry using indo-1 as intracellular Ca2+ probe. Galanin (0.1-1 nM) caused PRL and GH release coincident with a modest rise in [Ca2+]i. The increase in [Ca2+]i comprises the establishment of characteristic long-lasting bursts of [Ca2+]i transients. Galanin acts on Ca2+ entry through voltage-gated Ca2+ channels since there was no response to the peptide when Cd2(+)-a Ca2+ channel blocker-was added to the bath solution. The stimulation of bursting activity by galanin may provide a fine Ca2(+)-signalling mechanism which maximally stimulates hormone release while avoiding refractory periods.