The Veterinaire Principal Emile Decroix (1821-1901). Pioneer of struggle against tobacco

A l'occasion de la séance exceptionnelle de l'Académie Vétérinaire de France consacrée à « l'Homme, l'animal et le tabac », la vie et l'œuvre d'Emile Decroix, Vétérinaire militaire, méritaient d'être rappelées. Mu par une générosité sans limite alliée à une forte volonté qui lui feront sacrifier sa carrière et sa fortune, Decroix s'est dévoué à plusieurs actions philantropiques dont la lutte contre le tabac fut la principale. Fondateur des deux premières sociétés contre l'abus du tabac en 1868 et en 1877, son action de santé publique est aujourd'hui perpé tuée par celle du Comité National Contre le Tabagisme et l’émergence d'une prise de conscience collective sur les méfaits du tabac.On the occasion of an exceptional session of French Veterinary Academy which has been devoted to the following subject: "Man, Animal and Tobacco", the life and work of Emile Decroix was worth recalling. This French military Vet sacrificed his fortune and career to philan tropie works, chiefly struggler against the abuse of tobacco. He acted as a pioneer and founded the first two Societies against tobacco in 1868 and in 1877. His Public Health's program is still continueted with the "French National Comity against Tobacco's Abuse"

Effect of arsenic-phosphorus interaction on arsenic-induced oxidative stress in chickpea plants

Arsenic-induced oxidative stress in chickpea was investigated under glasshouse conditions in response to application of arsenic and phosphorus. Three levels of arsenic (0, 30 and 60 mg kg−1) and four levels of P (50, 100, 200, and 400 mg kg−1) were applied to soil-grown plants. Increasing levels of both arsenic and P significantly increased arsenic concentrations in the plants. Shoot growth was reduced with increased arsenic supply regardless of applied P levels. Applied arsenic induced oxidative stress in the plants, and the concentrations of H2O2 and lipid peroxidation were increased. Activity of superoxide dismutase (SOD) and concentrations of non-enzymatic antioxidants decreased in these plants, but activities of catalase (CAT) and ascorbate peroxidase (APX) were significantly increased under arsenic phytotoxicity. Increased supply of P decreased activities of CAT and APX, and decreased concentrations of non-enzymatic antioxidants, but the high-P plants had lowered lipid peroxidation. It can be concluded that P increased uptake of arsenic from the soil, probably by making it more available, but although plant growth was inhibited by arsenic the P may have partially protected the membranes from arsenic-induced oxidative stress

Anopheles gambiae PGRPLC-Mediated Defense against Bacteria Modulates Infections with Malaria Parasites

Recognition of peptidoglycan (PGN) is paramount for insect antibacterial defenses. In the fruit fly Drosophila melanogaster, the transmembrane PGN Recognition Protein LC (PGRP-LC) is a receptor of the Imd signaling pathway that is activated after infection with bacteria, mainly Gram-negative (Gram−). Here we demonstrate that bacterial infections of the malaria mosquito Anopheles gambiae are sensed by the orthologous PGRPLC protein which then activates a signaling pathway that involves the Rel/NF-κB transcription factor REL2. PGRPLC signaling leads to transcriptional induction of antimicrobial peptides at early stages of hemolymph infections with the Gram-positive (Gram+) bacterium Staphylococcus aureus, but a different signaling pathway might be used in infections with the Gram− bacterium Escherichia coli. The size of mosquito symbiotic bacteria populations and their dramatic proliferation after a bloodmeal, as well as intestinal bacterial infections, are also controlled by PGRPLC signaling. We show that this defense response modulates mosquito infection intensities with malaria parasites, both the rodent model parasite, Plasmodium berghei, and field isolates of the human parasite, Plasmodium falciparum. We propose that the tripartite interaction between mosquito microbial communities, PGRPLC-mediated antibacterial defense and infections with Plasmodium can be exploited in future interventions aiming to control malaria transmission. Molecular analysis and structural modeling provided mechanistic insights for the function of PGRPLC. Alternative splicing of PGRPLC transcripts produces three main isoforms, of which PGRPLC3 appears to have a key role in the resistance to bacteria and modulation of Plasmodium infections. Structural modeling indicates that PGRPLC3 is capable of binding monomeric PGN muropeptides but unable to initiate dimerization with other isoforms. A dual role of this isoform is hypothesized: it sequesters monomeric PGN dampening weak signals and locks other PGRPLC isoforms in binary immunostimulatory complexes further enhancing strong signals

The Effects Of N, P And Crude Oil On The Decomposition Of Spartina Alterniflora Belowground Biomass

We conducted a laboratory experiment to examine how the decomposition of particulate belowground organic matter from a salt marsh is enhanced, or not, by different mixtures of crude oil, nitrogen (N), or phosphorus (P) acting individually or synergistically. The experiment was conducted in 3.8 L sampling chambers producing varying quantities of gas whose volume was used as a surrogate measure of organic decomposition under anaerobic conditions. Gas production after 28 days, from highest to lowest, was +NP = +N \u3e\u3e\u3e +P, or +oil. The gas production under either +P or +oil conditions was indistinguishable from gas production in the control chamber. Nitrogen, not phosphorus, or +NP, was the dominant factor controlling organic decomposition rates in these experiments. The implication for organic salt marsh soils is that shoreline erosion is enhanced by salt marsh oiling, presumably by its toxicity, but not by its effect on the decomposition rates of plant biomass belowground. Nutrient additions, on the other hand, may compromise the soil strength, creating a stronger disparity in soil strength between upper and lower soil layers leading to marsh loss. Nutrient amendments intended to decrease oil concentration in the marsh may not have the desired effect, and are likely to decrease soil strength, thereby enhancing marsh-to-water conversions in organic salt marsh soils

Localization of a Guanylyl Cyclase to Chemosensory Cilia Requires the Novel Ciliary MYND Domain Protein DAF-25

In harsh conditions, Caenorhabditis elegans arrests development to enter a non-aging, resistant diapause state called the dauer larva. Olfactory sensation modulates the TGF-β and insulin signaling pathways to control this developmental decision. Four mutant alleles of daf-25 (abnormal DAuer Formation) were isolated from screens for mutants exhibiting constitutive dauer formation and found to be defective in olfaction. The daf-25 dauer phenotype is suppressed by daf-10/IFT122 mutations (which disrupt ciliogenesis), but not by daf-6/PTCHD3 mutations (which prevent environmental exposure of sensory cilia), implying that DAF-25 functions in the cilia themselves. daf-25 encodes the C. elegans ortholog of mammalian Ankmy2, a MYND domain protein of unknown function. Disruption of DAF-25, which localizes to sensory cilia, produces no apparent cilia structure anomalies, as determined by light and electron microscopy. Hinting at its potential function, the dauer phenotype, epistatic order, and expression profile of daf-25 are similar to daf-11, which encodes a cilium-localized guanylyl cyclase. Indeed, we demonstrate that DAF-25 is required for proper DAF-11 ciliary localization. Furthermore, the functional interaction is evolutionarily conserved, as mouse Ankmy2 interacts with guanylyl cyclase GC1 from ciliary photoreceptors. The interaction may be specific because daf-25 mutants have normally-localized OSM-9/TRPV4, TAX-4/CNGA1, CHE-2/IFT80, CHE-11/IFT140, CHE-13/IFT57, BBS-8, OSM-5/IFT88, and XBX-1/D2LIC in the cilia. Intraflagellar transport (IFT) (required to build cilia) is not defective in daf-25 mutants, although the ciliary localization of DAF-25 itself is influenced in che-11 mutants, which are defective in retrograde IFT. In summary, we have discovered a novel ciliary protein that plays an important role in cGMP signaling by localizing a guanylyl cyclase to the sensory organelle

Relationship between inpatient satisfaction and nurse absenteeism: an exploratory study using WHO-PATH performance indicators in France

<p>Abstract</p> <p>Background</p> <p>Indicators describing results of care are widely explored in term of patient satisfaction (PS). Among factors explaining PS, human resources indicators have been studied in terms of burnout or job satisfaction among healthcare professionals. No research work has set out to explore the effect of absenteeism on PS scores. The objective of this study was to explore interaction between rate of absenteeism among nurses and PS results.</p> <p>Methods</p> <p>France has taken part in a project named PATH (Performance Assessment Tool for Hospitals) of the World Health Organization, aiming to develop a tool for the assessment of hospital performance. In the first semester 2008, 25 volunteering short-stay hospitals (teaching, general and private) provide complete data on nurse short-absenteeism (periods of up to 7 consecutive days of sick leave) and on PS (a cross-sectional postal survey using a standardized validated French-language scale EQS-H exploring "quality of medical information" (MI) and "relationships with staff and daily routine" (RS)). A multi-level model was used to take into account of the hierarchical nature of the data.</p> <p>Results</p> <p>Two thousand and sixty-five patients responded to the satisfaction questionnaire (participation rate: 40.9%). The mean age of respondents was 58 yrs (± 19), 41% were men. The mean duration of hospitalisation was 7.5 days (± 11.1). The mean absenteeism rate for nurses was 0.24% (± 0.14).</p> <p>All the PS scores were significantly and negatively correlated with rate of short-absenteeism among nurses (MI score: <it>ρ </it>= -0.55, <it>p </it>< 0.01), RS score <it>ρ </it>= -0.47, <it>p </it>= 0.02). The mixed model found a significant relationship between rate of absenteeism among nurses and PS scores (MI: <it>p </it>= 0.027; RS: <it>p </it>= 0.017).</p> <p>Conclusion</p> <p>Results obtained in this study show that short-term absenteeism among nurses seems to be significantly and negatively correlated with PS. Our findings are an invitation to deepen our understanding of the impact of human resources on PS and to develop more specific projects.</p

Macoilin, a Conserved Nervous System–Specific ER Membrane Protein That Regulates Neuronal Excitability

Genome sequence comparisons have highlighted many novel gene families that are conserved across animal phyla but whose biological function is unknown. Here, we functionally characterize a member of one such family, the macoilins. Macoilins are characterized by several highly conserved predicted transmembrane domains towards the N-terminus and by coiled-coil regions C-terminally. They are found throughout Eumetazoa but not in other organisms. Mutants for the single Caenorhabditis elegans macoilin, maco-1, exhibit a constellation of behavioral phenotypes, including defects in aggregation, O2 responses, and swimming. MACO-1 protein is expressed broadly and specifically in the nervous system and localizes to the rough endoplasmic reticulum; it is excluded from dendrites and axons. Apart from subtle synapse defects, nervous system development appears wild-type in maco-1 mutants. However, maco-1 animals are resistant to the cholinesterase inhibitor aldicarb and sensitive to levamisole, suggesting pre-synaptic defects. Using in vivo imaging, we show that macoilin is required to evoke Ca2+ transients, at least in some neurons: in maco-1 mutants the O2-sensing neuron PQR is unable to generate a Ca2+ response to a rise in O2. By genetically disrupting neurotransmission, we show that pre-synaptic input is not necessary for PQR to respond to O2, indicating that the response is mediated by cell-intrinsic sensory transduction and amplification. Disrupting the sodium leak channels NCA-1/NCA-2, or the N-,P/Q,R-type voltage-gated Ca2+ channels, also fails to disrupt Ca2+ responses in the PQR cell body to O2 stimuli. By contrast, mutations in egl-19, which encodes the only Caenorhabditis elegans L-type voltage-gated Ca2+ channel α1 subunit, recapitulate the Ca2+ response defect we see in maco-1 mutants, although we do not see defects in localization of EGL-19. Together, our data suggest that macoilin acts in the ER to regulate assembly or traffic of ion channels or ion channel regulators

Iodine doped carbon nanotube cables exceeding specific electrical conductivity of metals

Creating highly electrically conducting cables from macroscopic aggregates of carbon nanotubes, to replace metallic wires, is still a dream. Here we report the fabrication of iodine-doped, double-walled nanotube cables having electrical resistivity reaching ∼10−7 Ω.m. Due to the low density, their specific conductivity (conductivity/weight) is higher than copper and aluminum and is only just below that of the highest specific conductivity metal, sodium. The cables exhibit high current-carrying capacity of 104∼105 A/cm2 and can be joined together into arbitrary length and diameter, without degradation of their electrical properties. The application of such nanotube cables is demonstrated by partly replacing metal wires in a household light bulb circuit. The conductivity variation as a function of temperature for the cables is five times smaller than that for copper. The high conductivity nanotube cables could find a range of applications, from low dimensional interconnects to transmission lines

Prominent and Persistent Extraneural Infection in Human PrP Transgenic Mice Infected with Variant CJD

Background. The evolution of the variant Creutzfeldt-Jakob disease (vCJD) epidemic is hazardous to predict due to uncertainty in ascertaining the prevalence of infection and because the disease might remain asymptomatic or produce an alternate, sporadic-like phenotype. Methodology/Principal Findings. Transgenic mice were produced that overexpress human prion protein with methionine at codon 129, the only allele found so far in vCJD-affected patients. These mice were infected with prions derived from variant and sporadic CJD (sCJD) cases by intracerebral or intraperitoneal route, and transmission efficiency and strain phenotype were analyzed in brain and spleen. We showed that i) the main features of vCJD infection in humans, including a prominent involvement of the lymphoid tissues compared to that in sCJD infection were faithfully reproduced in such mice; ii) transmission of vCJD agent by intracerebral route could lead to the propagation of either vCJD or sCJD-like prion in the brain, whereas vCJD prion was invariably propagated in the spleen, iii) after peripheral exposure, inefficient neuroinvasion was observed, resulting in an asymptomatic infection with life-long persistence of vCJD prion in the spleen at stable and elevated levels. Conclusion/Significance. Our findings emphasize the possibility that human-to-human transmission of vCJD might produce alternative neuropathogical phenotypes and that lymphoid tissue examination of CJD cases classified as sporadic might reveal an infection by vCJD-type prions. They also provide evidence for the strong propensity of this agent to establish long-lasting, subclinical vCJD infection of lymphoreticular tissues, thus amplifying the risk for iatrogenic transmission

Effective Gene Therapy in a Mouse Model of Prion Diseases

Classical drug therapies against prion diseases have encountered serious difficulties. It has become urgent to develop radically different therapeutic strategies. Previously, we showed that VSV-G pseudotyped FIV derived vectors carrying dominant negative mutants of the PrP gene are efficient to inhibit prion replication in chronically prion-infected cells. Besides, they can transduce neurons and cells of the lymphoreticular system, highlighting their potential use in gene therapy approaches. Here, we used lentiviral gene transfer to deliver PrPQ167R virions possessing anti-prion properties to analyse their efficiency in vivo. Since treatment for prion diseases is initiated belatedly in human patients, we focused on the development of a curative therapeutic protocol targeting the late stage of the disease, either at 35 or 105 days post-infection (d.p.i.) with prions. We observed a prolongation in the lifespan of the treated mice that prompted us to develop a system of cannula implantation into the brain of prion-infected mice. Chronic injections of PrPQ167R virions were done at 80 and 95 d.p.i. After only two injections, survival of the treated mice was extended by 30 days (20%), accompanied by substantial improvement in behaviour. This delay was correlated with: (i) a strong reduction of spongiosis in the ipsilateral side of the brain by comparison with the contralateral side; and (ii) a remarkable decrease in astrocytic gliosis in the whole brain. These results suggest that chronic injections of dominant negative lentiviral vectors into the brain, may be a promising approach for a curative treatment of prion diseases