Direct and deferred sediment-transport events and seafloor disturbance induced by trawling in submarine canyons.

Bottom trawling on marine environments can drastically modify seafloor geomorphology and sedimentary dynamics not only on the fishing grounds but also in adjacent downslope regions, particularly in submarine canyons environments, which are hotspots of benthic biomass and productivity in the deep sea. When this type of fishery occurs along submarine canyon flanks, it can induce sediment gravity flows that descend along tributary gullies towards the main canyon axis. However, these flows had only been clearly identified in the Palamós Canyon, where they could be recorded synchronously with the passage of the trawling fleet. In this study we also recorded trawl-induced sediment gravity flows in the Blanes Canyon, both synchronously and asynchronously with the passage of trawlers. Increases in particulate matter fluxes in other trawled submarine canyons occurring in absence of natural triggering mechanisms, were not directly associated with bottom trawling because of the lack of direct synchronicity of these events with this human activity. Here we show, however, that the practice of bottom trawling along canyon flanks can not only resuspend and directly trigger sediment gravity flows, but they can also pile up disturbed sediment on steep areas, which can become unstable and collapse afterwards, asynchronically with the passage of trawlers. Our study provides evidence that sediment gravity flows in submarine canyons affected by bottom trawling, where the causal mechanisms are presently unidentified, may potentially be linked to instabilities in sediment originating from recurrent bottom trawling, which can precondition these events.

Assessing the impact of the global subsea telecommunications network on sedimentary organic carbon stocks.

The sequestration of organic carbon in seafloor sediments plays a key role in regulating global climate; however, human activities can disturb previously-sequestered carbon stocks, potentially reducing the capacity of the ocean to store CO2. Recent studies revealed profound seafloor impacts and sedimentary carbon loss due to fishing and shipping, yet most other human activities in the ocean have been overlooked. Here, we present an assessment of organic carbon disturbance related to the globally-extensive subsea telecommunications cable network. Up to 2.82-11.26 Mt of organic carbon worldwide has been disturbed as a result of cable burial, in water depths of up to 2000 m. While orders of magnitude lower than that disturbed by bottom fishing, it is a non-trivial amount that is absent from global budgets. Future offshore developments that disturb the seafloor should consider the safeguarding of carbon stocks, across the full spectrum of Blue Economy industries.

Of logos and men: semantic memory impairment for unique entities in a case of semantic variant of primary progressive aphasia.

In this study, an individual (NG) with the semantic varient of primary progressive aphasis (svPPA) was assessed with tasks designed to investigate the recognition and activation of semantic knowledge about unique entities. NG had significant difficulties in the recognition of brand names and famous names but was largely unimpaired in the recognition of logos and famous faces. However, she was impaired in tasks requiring the activation of semantic representations of logos, brand names, famous faces, and famous names. These results suggest that the recognition of unique entities results from the interaction of perceptual and conceptual processes and, that the ability to activate semantic information about these entities can be affected in svPPA.

Preconception care among low-risk mothers in a French perinatal network: Frequency of utilization and factors associated.

OBJECTIVE: Determine the frequency of preconception care use in France and factors impacting preconception visit. MATERIALS AND METHODS: An epidemiological study was conducted from September 2015 to October 2015 in 5 maternity hospitals within the "Alpes-Isère" perinatal network, comprising of French-speaking women, with uncomplicated pregnancies, who delivered a healthy term baby (≥37 weeks of gestational age). Two groups were compared: patients with and without preconception care. Descriptive, univariate and multivariate analyses were performed for the sociodemographic, the environmental characteristics and the gynecologic obstetric history. RESULTS: Among the 392 patients included in this study, only 62 (15.8% [12.0-20.0]) had used preconception care before their pregnancy. Multivariate analysis showed that the primiparous women (adjusted OR 2.47 [1.37-4.46]) and the women with a high socio-professional category (adjusted OR 2.32 [1.13-4.77]) were more likely to used preconception care. CONCLUSION: Despite the positive effects on mother and baby's health, preconception care is insufficiently used in France. Every effort must be made to improve awareness of preconception care among health workers and patients.

[Skeletal muscle ischemia-reperfusion and ischemic conditioning pathophysiology-clinical applications for the vascular surgeon]. / Physiopathologie de l'ischémie-reperfusion et du conditionnement ischémique du muscle squelettique ­ applications cliniques pour le chirurgien vasculaire.

Ischemia-reperfusion, which is characterized by deficient oxygen supply and subsequent restoration of blood flow, can cause irreversible damage to tissue. The vascular surgeon is daily faced with ischemia-reperfusion situations. Indeed, arterial clamping induces ischemia, followed by reperfusion when declamping. Mechanisms underlying ischemia-reperfusion injury are complex and multifactorial. Increases in cellular calcium and reactive oxygen species, initiated during ischemia and then amplified upon reperfusion are thought to be the main mediators of reperfusion injury. Mitochondrial dysfunction also plays an important role. Extensive research has focused on increasing skeletal muscle tolerance to ischemia-reperfusion injury, especially through the use of ischemic conditioning strategies. The purpose of this review is to focus on the cellular responses associated with ischemia-reperfusion, as well as to discuss the effects of ischemic conditioning strategies. This would help the vascular surgeon in daily practice, in order to try to improve surgical outcome in the setting of ischemia-reperfusion.

Inhibition of mitochondrial membrane permeability as a putative pharmacological target for cardioprotection.

Myocardial ischemia-reperfusion injury is a major cause of morbidity and mortality in developed countries. To date, the only treatment of complete ischemia is to restore blood flow; thus the search for new cardioprotective approaches is absolutely necessary to reduce the mortality associated with myocardial ischemia. Ischemia has long been considered to result in necrotic tissue damage but the reduction in oxygen supply can also lead to apoptosis. Therefore, in the last few years, mitochondria have become the subject of growing interest in myocardial ischemia-reperfusion since they are strongly involved in the regulation of the apoptotic process. Indeed, during ischemia-reperfusion, pathological signals converge in the mitochondria to induce permeabilization of the mitochondrial membrane. Two classes of mechanisms, which are not mutually exclusive, emerged to explain mitochondrial membrane permeabilization. The first occurs via a non-specific channel known as the mitochondrial permeability transition pore (mPTP) in the inner and the outer membranes causing disruption of the impermeability of the inner membrane, and ultimately complete inhibition of mitochondrial function. The second mechanism, involving only the outer membrane, induces the release of cell death effectors. Thus, drugs able to block or to limit mitochondrial membrane permeabilization may be cytoprotective during ischemia-reperfusion. The objective of this review is to examine the pharmacological strategies capable of inhibiting mitochondrial membrane permeabilization induced by myocardial ischemia-reperfusion.

Calcium deficiency cannot induce obesity in rats.

If intake of a required nutrient--here calcium--affects body weight, the effect must be mediated by a change in the body weight set-point. Thus, the controversial 'anti-obesity' influence of high calcium intake should decrease the body weight set-point. Diets differing in calcium content were assigned to three groups of rats. The effects of the diets on body weight, BMI, fat content, plasma calcium, body weight set-point, food intake, and preference for various calcium solutions were measured after 6 weeks of calcium deprivation or supplementation, and again after a further 6 weeks of recovery on a regular diet. After 6 weeks, the low-calcium diet had induced calcium deficiency but had failed to raise the body weight set-point. Nor had it produced obesity or fat accumulation. After 6 weeks of recovery, body weight and fat content were no higher in calcium-deprived rats than in the control or supplemented rats. In this experiment, low-calcium intake failed to cause obesity and did not raise the body weight set-point. The results indicate that calcium intake probably does not affect body weight.

Oral anticoagulation thresholds.

BACKGROUND: Monitoring patients on oral anticoagulation is essential to prevent hemorrhage and recurrent thrombosis. We studied tissue factor-induced whole-blood coagulation in patients on warfarin therapy with similar international normalized ratios (INRs). METHODS AND RESULTS: Contact pathway-suppressed whole-blood coagulation initiated with tissue factor was studied in 8 male subjects (group W) and in 1 individual multiple times (subject A). Coagulation profiles for group W showed that subjects with similar INRs had widely varying clot times (6.2 to 23 minutes) and thrombin-antithrombin III (TAT) profiles with rates of 25 to 40 nmol. L(-1). min(-1) and maximum levels varying from 192 to 349 nmol/L. The normal control group exhibited clot times of 5.7+/-0.3 minutes and TAT rates of 57+/-13 nmol. L(-1). min(-1), reaching maximum levels of 742+/-91 nmol/L. Subject A, who was stably anticoagulated at an INR of 2.1+/-0.4 for 6 months, had widely ranging profiles with clot times of 9.0 to 22.7 minutes, TAT maximums varying from 141 to 345 nmol/L, and TAT formation rates of 10 to 57 nmol. L(-1). min(-1). INR did not correlate with TAT formation. Platelet activation was decreased by anticoagulants but also displayed variability. Fibrinopeptide A generation showed threshold variability independent of the INR. Factor VIII levels were increased (P=0.03) in group W (204+/-34.4%) compared with normal control subjects (149.4+/-37.4%). A significant correlation was identified between increasing factor VIII levels and years on warfarin therapy (r=0.78, P=0.01), suggesting a possible factor VIII compensatory mechanism. CONCLUSIONS: These results suggest that control of anticoagulation in patients to a set INR therapeutic range may be less secure than anticipated. Patients with similar INRs show significant individual variability in their tissue factor coagulation response, suggesting different risks to anticoagulation when confronted with underlying vascular anomalies.

Homeostatic control of presynaptic release is triggered by postsynaptic membrane depolarization.

Homeostatic mechanisms regulate synaptic function to maintain nerve and muscle excitation within reasonable physiological limits. The mechanisms that initiate homeostasic changes to synaptic function are not known. We specifically impaired cellular depolarization by expressing the Kir2.1 potassium channel in Drosophila muscle. In Kir2.1-expressing muscle there is a persistent outward potassium current ( approximately 10 nA), decreased muscle input resistance (50-fold), and a hyperpolarized resting potential. Despite impaired muscle excitability, synaptic depolarization of muscle achieves wild-type levels. A quantal analysis demonstrates that increased presynaptic release (quantal content), without a change in quantal size (mEPSC amplitude), compensates for altered muscle excitation. Because morphological synaptic growth is normal, we conclude that a homeostatic increase in presynaptic release compensates for impaired muscle excitability. These data demonstrate that a monitor of muscle membrane depolarization is sufficient to initiate synaptic homeostatic compensation.

Development of a PCR assay for identification of staphylococci at genus and species levels.

We have developed a PCR-based assay which allows the detection of staphylococci at the genus level by targeting the tuf gene, which encodes the elongation factor Tu. Degenerate PCR primers derived from consensus regions of several tuf genes were used to amplify a target region of 884 bp from 11 representative staphylococcal species. Subsequently, the entire nucleotide sequence of these amplicons was determined. The analysis of a multiple alignment of these sequences revealed regions conserved among staphylococci but distinct from those of other gram-positive bacteria genetically related to staphylococci. PCR primers complementary to these regions could amplify specifically and efficiently a DNA fragment of 370 bp for all of 27 different staphylococcal species tested. There was no amplification with genomic DNA prepared from 53 nonstaphylococcal species tested to verify the specificity of the assay (20 gram positive and 33 gram negative). Furthermore, this assay amplified efficiently all 27 American Type Culture Collection (ATCC) staphylococcal reference strains as well as 307 clinical isolates of staphylococci from the Québec City region. Analysis of the multiple sequence alignment for the 884-bp fragment for the 11 staphylococcal species as well as comparison of the sequences for the 370-bp amplicon from five unrelated ATCC and clinical strains for each of the species S. aureus, S. epidermidis, S. haemolyticus, S. hominis, and S. saprophyticus demonstrated sufficient interspecies polymorphism to generate genus- and species-specific capture probes. This sequence information allowed the development of Staphylococcus-specific and species-specific (targeting S. aureus, S. epidermidis, S. haemolyticus, S. hominis, or S. saprophyticus) capture probes hybridizing to the 370-bp amplicon. In conclusion, this PCR assay is suitable for detection of staphylococci at both genus and species levels.

Inhibition of adherence of Actinobacillus pleuropneumoniae to porcine respiratory tract cells by monoclonal antibodies directed against LPS and partial characterization of the LPS receptors.

Actinobacillus pleuropneumoniae is the causative agent of porcine fibrinohemorrhagic necrotizing pleuropneumonia. We have previously identified the lipopolysaccharides (LPS) as the major adhesin of A. pleuropneumoniae involved in adherence to porcine respiratory tract cells. In the present study, adherence of A. pleuropneumoniae to porcine tracheal frozen sections was inhibited by homologous monovalent Fab fragments produced from monoclonal antibodies 5.1 G8F10 and 102-G02 directed, respectively, against the A. pleuropneumoniae serotype 1 or serotype 2 O-antigens. These results confirm the important role played by LPS in adherence of A. pleuropneumoniae and suggest that these adhesins might represent good vaccine candidates. We also investigated the presence of A. pleuropneumoniae receptors in tracheal cell preparations from piglets of four different breeds. Using Far-Western binding assays, we identified proteins recognized by whole cells of A. pleuropneumoniae reference strains for serotype 1 and 2, and local isolates belonging to the same serotypes, and also recognized by extracted LPS from both reference strains. We confirmed the proteinaceous nature of these LPS-binding molecules by their staining with Coomassie brilliant blue, sensitivity to proteinase K digestion, resistance to sodium m-periodate oxidation, and their inability to stain with glycoprotein-specific reagents. Four low-molecular-mass bands (14-17 kDa) seemed to correspond to histones. We also identified proteins at Mr 38,500 that could represent putative receptors for A. pleuropneumoniae LPS in swine respiratory tract cells.

Binding of Actinobacillus pleuropneumoniae lipopolysaccharides to glycosphingolipids evaluated by thin-layer chromatography.

The binding profile of Actinobacillus pleuropneumoniae serotypes 1 and 2 to various glycosphingolipids was evaluated by using thin-layer chromatogram overlay. A. pleuropneumoniae whole cells recognized glucosylceramide (Glcbeta1Cer), galactosylceramide (Galbeta1Cer) with hydroxy and nonhydroxy fatty acids, sulfatide (SO(3)-3Galbeta1Cer), lactosylceramide (Galbeta1-4Glcbeta1Cer), gangliotriaosylceramide GgO3 (GalNAcbeta1-4Galbeta1-4Glcbeta1Cer), and gangliotetraosylceramide GgO4 (Galbeta1-3GalNAcbeta1-4Galbeta1-4Glcbeta1Cer) glycosphingolipids. We observed no binding to globoseries, globotriaosylceramide Gb3, globoside Gb4, or Forssman Gb5 glycosphingolipids or to gangliosides GM1, GM2, GM3, GD1a, GD1b, GD3, and GT1b. The A. pleuropneumoniae strains tested also failed to detect phosphatidylethanolamine or ceramide. Interestingly, extracted lipopolysaccharide (LPS) of serotype 1 and serotype 2 as well as detoxified LPS of serotype 1 showed binding patterns similar to that of whole bacterial cells. Binding to GlcCer, GalCer, sulfatide, and LacCer, but not to GgO3 and GgO4 glycosphingolipids, was inhibited after incubation of the bacteria with monoclonal antibodies against LPS O antigen. These findings indicate the involvement of LPS in recognition of three groups of glycosphingolipids: (i) GlcCer and LacCer, where glucose is probably an important saccharide sequence required for LPS binding; (ii) GalCer and sulfatide glycosphingolipids, where the sulfate group is part of the binding epitope of the isoreceptor; and (iii) GgO3 and GgO4, where GalNacbeta1-4Gal disaccharide represents the minimal common binding epitope. Taken together, our results indicate that A. pleuropneumoniae LPS recognize various saccharide sequences found in different glycosphingolipids, which probably represents a strong virulence attribute.

A PDK1 homolog is necessary and sufficient to transduce AGE-1 PI3 kinase signals that regulate diapause in Caenorhabditis elegans.

An insulin receptor-like signaling pathway regulates Caenorhabditis elegans metabolism, development, and longevity. Inactivation of the insulin receptor homolog DAF-2, the AGE-1 PI3K, or the AKT-1 and AKT-2 kinases causes a developmental arrest at the dauer stage. A null mutation in the daf-16 Fork head transcription factor alleviates the requirement for signaling through this pathway. We show here that a loss-of-function mutation in pdk-1, the C. elegans homolog of the mammalian Akt/PKB kinase PDK1, results in constitutive arrest at the dauer stage and increased life span; these phenotypes are suppressed by a loss of function mutation in daf-16. An activating mutation in pdk-1 or overexpression of wild-type pdk-1 relieves the requirement for AGE-1 PI3K signaling. Therefore, pdk-1 activity is both necessary and sufficient to propagate AGE-1 PI3K signals in the DAF-2 insulin receptor-like signaling pathway. The activating mutation in pdk-1 requires akt-1 and akt-2 gene activity in order to suppress the dauer arrest phenotype of age-1. This indicates that the major function of C. elegans PDK1 is to transduce signals from AGE-1 to AKT-1 and AKT-2. The activating pdk-1 mutation is located in a conserved region of the kinase domain; the equivalent amino acid substitution in human PDK1 activates its kinase activity toward mammalian Akt/PKB.

Caenorhabditis elegans Akt/PKB transduces insulin receptor-like signals from AGE-1 PI3 kinase to the DAF-16 transcription factor.

A neurosecretory pathway regulates a reversible developmental arrest and metabolic shift at the Caenorhabditis elegans dauer larval stage. Defects in an insulin-like signaling pathway cause arrest at the dauer stage. We show here that two C. elegans Akt/PKB homologs, akt-1 and akt-2, transduce insulin receptor-like signals that inhibit dauer arrest and that AKT-1 and AKT-2 signaling are indispensable for insulin receptor-like signaling in C. elegans. A loss-of-function mutation in the Fork head transcription factor DAF-16 relieves the requirement for Akt/PKB signaling, which indicates that AKT-1 and AKT-2 function primarily to antagonize DAF-16. This is the first evidence that the major target of Akt/PKB signaling is a transcription factor. An activating mutation in akt-1, revealed by a genetic screen, as well as increased dosage of wild-type akt-1 relieves the requirement for signaling from AGE-1 PI3K, which acts downstream of the DAF-2 insulin/IGF-1 receptor homolog. This demonstrates that Akt/PKB activity is not necessarily dependent on AGE-1 PI3K activity. akt-1 and akt-2 are expressed in overlapping patterns in the nervous system and in tissues that are remodeled during dauer formation.

Adhesin-receptor interactions in Pasteurellaceae.

The ability of bacteria to adhere to mucosal epithelium is dependent on the expression of adhesive molecules or structures, called adhesins, that allow attachment of the organisms to complementary molecules on mucosal surfaces, the receptors. Important human and animal pathogens are found among the Pasteurellaceae family which includes Haemophilus, Actinobacillus, and Pasteurella organisms. The purpose of this paper is to review the adhesin-receptor systems found in Pasteurellaceae, with an emphasis on recent developments in this specific area. Most of these organisms can employ multiple molecular mechanisms of adherence (or multiple adhesins) to initiate infection. Indeed, a wide variety of adhesins are expressed by members of the Pasteurellaceae, and different proteins (e.g. fimbriae, fibrils, outer membrane proteins) as well as polysaccharides (lipooligosaccharides, lipopolysaccharides, capsular polysaccharides) were clearly shown to play an important role in adherence. In many instances, these adhesins have proved to represent good vaccine candidates. Surprisingly, the receptors on host mucosal surfaces have yet been identified in very few cases.

Northern exposure: further analysis of the results of the Canadian aboriginal methylmercury program.

An initial overall analysis of the Canadian First Nations and Inuit data on methylmercury (MeHg) levels in 38,571 Canadian Aboriginal people has been completed. Patterns of exposure and their relationship to socio-cultural issues and traditional lifestyles are now being further analyzed, especially in the light of the continuing concern regarding the significance of exposure among northern and arctic populations. A mean of 29.8 micrograms/l mercury in blood or blood equivalent, with a range of 1-225.7 micrograms/l, was found among Inuit in the Northwest Territories (NWT). Significant differences in South-North exposure and West-East exposure in NWT are discussed, as are the relationships between exposure of northern residents and development activities further south, and problems of risk management in the context of traditional arctic lifestyles. It is suggested that many of the differences are due to the greater consumption of traditional food in the North. However, with the levels found and current state of knowledge, this should not be seen as a reason to change lifestyles--a change which carries its own negative consequences.

The Fork head transcription factor DAF-16 transduces insulin-like metabolic and longevity signals in C. elegans.

In mammals, insulin signalling regulates glucose transport together with the expression and activity of various metabolic enzymes. In the nematode Caenorhabditis elegans, a related pathway regulates metabolism, development and longevity. Wild-type animals enter the developmentally arrested dauer stage in response to high levels of a secreted pheromone, accumulating large amounts of fat in their intestines and hypodermis. Mutants in DAF-2 (a homologue of the mammalian insulin receptor) and AGE-1 (a homologue of the catalytic subunit of mammalian phosphatidylinositol 3-OH kinase) arrest development at the dauer stage. Moreover, animals bearing weak or temperature-sensitive mutations in daf-2 and age-1 can develop reproductively, but nevertheless show increased energy storage and longevity. Here we show that null mutations in daf-16 suppress the effects of mutations in daf-2 or age-1; lack of daf-16 bypasses the need for this insulin receptor-like signalling pathway. The principal role of DAF-2/AGE-1 signalling is thus to antagonize DAF-16. daf-16 is widely expressed and encodes three members of the Fork head family of transcription factors. The DAF-2 pathway acts synergistically with the pathway activated by a nematode TGF-beta-type signal, DAF-7, suggesting that DAF-16 cooperates with nematode SMAD proteins in regulating the transcription of key metabolic and developmental control genes. The probable human orthologues of DAF-16, FKHR and AFX, may also act downstream of insulin signalling and cooperate with TGF-beta effectors in mediating metabolic regulation. These genes may be dysregulated in diabetes.

Identification of two core types in lipopolysaccharides of Actinobacillus pleuropneumoniae representing serotypes 1 to 12.

Lipopolysaccharides (LPS) of Actinobacillus pleuropneumoniae were separated by Tricine-SDS-polyacrylamide gel electrophoresis, which has been shown to improve resolution of low-molecular-mass fast migrating bands. Strains representing the 12 serotypes of A. pleuropneumoniae can be divided in two groups according to the gel mobility of the core - lipid A region of their LPS. The first electromorphic core type (core type I), found in serotypes 1, 6, 9, and 11, had a migration slower than Salmonella typhimurium Ra LPS. The second electromorphic core type (core type II), found in the remaining serotypes (i.e., 2, 3, 4, 5, 7, 8, 10, and 12) had a migration similar to S. typhimurium Ra LPS. Furthermore, we observed that these two core types were antigenically different. Western blot analyses indicated that core - lipid A region of LPS from electromorphic core type I strains reacted when probed with serum from a pig experimentally infected with a core type I strain but not when probed with serum from a pig experimentally infected with a core type II strain. Conversely, core - lipid A region of LPS from electromorphic core type II strains reacted only when probed with serum from a pig experimentally infected with a core type II strain. Our results, based on both electrophoretic mobility and antigenicity, suggest the presence of two LPS core types in A. pleuropneumoniae.

Examination of surface polysaccharides of Actinobacillus pleuropneumoniae serotype 1 grown under iron-restricted conditions.

We investigated the expression of important Actinobacillus pleuropneumoniae surface polysaccharides, namely, capsular polysaccharides (CPS) and lipopolysaccharides (LPS), after growth under iron-restricted conditions. Iron restriction did not seem to affect the production of CPS, as determined by labelling with a monoclonal antibody (mAb) against the serotype 1 K-antigen and flow cytometry analysis, and also as determined by electron microscopy. SDS-PAGE revealed that the LPS profiles of these cells were also unaffected by iron restriction. Using flow cytometry analysis, however, we observed that binding of mAb against serotype 1 O-antigen was altered in cells of A. pleuropneumoniae serotype 1 reference strain (4074) grown under iron-restricted conditions. This strain exhibited two subpopulations with distinct patterns of reactivity with the mAb against the O-antigen. When strain 4074 was grown under iron-restricted conditions, a shift from one cell subpopulation (moderately fluorescent) to another cell subpopulation (highly fluorescent, thus binding more antibodies) was observed. Our results indicate that growth of A. pleuropneumoniae serotype 1 under iron-restricted conditions did not seem to affect CPS production, but might alter, at least for the reference strain, the expression of LPS.