Active oceanic spreading in the northern north Fiji basin : results of the NOFI cruise of R/V l'Atalante (Newstarmer project)

The South Pandora and the Tripartite Ridges are active spreading centers located in the northern part of the North Fiji Basin. These spreading centers were surveyed over a distance of 750 km during the NOFI cruise of R/V L'Atalante (August-September 1994) which was conducted in the frame of the french-japanese Newstarmer cooperation project. SIMRAD EM12-dual full coverage swath bathymetric and imagery data as well as airgun 6-channel seismic, magnetics and gravity profiles were recorded along an off-axis from 170°40'E to 178°E. Dredging and piston coring were also performed along and off-axis. The axial domain of the South Pandora Ridge is divided into 5 first-order segments characterized by contrasted morphologies. The average width of the active domain is 20 km and corresponds either to bathymetric highs or to deep elongated grabens. The bathymetric highs are volcanic constructions, locally faulted and rifted, which can obstruct totally the axial valley. The grabens show the typical morphology of slow spreading axes, with two steep walls flanking a deep axial valley. Elongated lateral ridges may be present on both sides of the grabens. Numerous volcanoes, up to several kilometers in diameter, occur on both flanks of the South Pandora Ridge. The Tripartite Ridge consists of three main segments showing a sigmoid shape. Major changes in the direction of the active zones are observed at the segment discontinuities. These discontinuities show various geometrical patterns which suggest complex transform relay zones. Preliminary analysis of seismic reflection profiles suggest that the Tripartite Ridge is a very young feature which propagates into an older oceanic domain characterized by a significant sedimentary cover. By contrast, a very thin to absent sedimentary cover is observed about 100 km on both flanks of the South Pandora Ridge active axis. The magnetic anomaly profiles give evidence of long and continuous lineations, parallel to the South Pandora Ridge spreading axis. (Résumé d'auteur

The genetic basis of multiple sclerosis: a model for MS susceptibility

<p>Abstact</p> <p>Background</p> <p>MS-pathogenesis is known to involve both multiple environmental events, and several independent genetic risk-factors.</p> <p>Methods</p> <p>A model of susceptibility is developed and a mathematical analysis undertaken to elucidate the nature of genetic susceptibility to MS and to understand the constraints that are placed on the genetic basis of MS, both by the known epidemiological facts of this disease and by the known frequency of the HLA DRB1*1501 allele in the general populations of northern Europe and North America.</p> <p>Results</p> <p>For the large majority of cases (possibly all), MS develops, in part, because an individual is genetically susceptible. Nevertheless, 2.2% or less of the general population is genetically susceptible. Moreover, from the model, the number of susceptibility-loci that need to be in a "susceptible allelic state" to produce MS-susceptibility is small (11-18), whereas the total number of such susceptibility-loci is large (50-200), and their "frequency of susceptibility" is low (i.e., ≤ 0.12). The optimal solution to the model equations (which occurs when 80% of the loci are recessive) predicts the epidemiological data quite closely.</p> <p>Conclusions</p> <p>The model suggests that combinations of only a small number of genetic loci in a "susceptible allelic state" produce MS-susceptibility. Nevertheless, genome-wide associations studies with hundreds of thousands of SNPs, are plagued by both false-positive and false-negative identifications and, consequently, emphasis has been rightly placed on the replicability of findings. Nevertheless, because genome-wide screens don't distinguish between true susceptibility-loci and disease-modifying-loci, and because only true susceptibility-loci are constrained by the model, unraveling the two will not be possible using this approach.</p> <p>The model also suggests that HLA DRB1 may not be as uniquely important for MS-susceptibility as currently believed. Thus, this allele is only one among a hundred or more loci involved in MS susceptibility. Even though the "frequency of susceptibility" at the HLA DRB1 locus is four-fold that of other loci, the penetrance of those susceptible genotypes that include this allele is no different from those that don't. Also, almost 50% of genetically-susceptible individuals, lack this allele. Moreover, of those who have it, only a small fraction (≤ 5.2%) are even susceptible to getting MS.</p

Influence of gel bentonite on physiological indicators of the white laboratory mice.

The evaluation of the effect of lifelong usage of sodium form of gel bentonite on some physiological parameters of mice (body weight, feed and water intake, general condition, change in coordination of movements, state of wool, fertility and mortality) was performed on 110 white laboratory mice (BALB / c line). This experimental study was carried out in two replicates. To accomplish this task, the mice were divided into two groups: control – the animals were on a standard diet, and experimental – they used water with the addition of sodium form of bentonite gel (0.5-1%). It was found that prolonged intake of bentonite gel by laboratory animals neither led to an excessive increase in their weight (the weight gain of the experimental group did not differ statistically significantly from the control group, p≤0.05), nor did it cause acute or chronic intoxication. It is also shown that the constant use of bentonite has a positive effect on the organism of experimental mice, which is expressed in the decrease of animal mortality, increase of life expectancy and pronounced positive effect on fertility functions (increase in the number of offspring). Based on the obtained data it can be assumed that the continuous intake of bentonite by the animal organism is one of the factors of their microbiome improvement, which affects on a plenty of physiological functions, including animals reproduction. It is possible that smectite sorbents also enrich the body of mice by certain essential mineral elements (silicon, etc.) and has cytomucoprotective properties concerning the mucous membranes of the macroorganism

Influence of gel bentonite on physiological indicators of the white laboratory mice.

The evaluation of the effect of lifelong usage of sodium form of gel bentonite on some physiological parameters of mice (body weight, feed and water intake, general condition, change in coordination of movements, state of wool, fertility and mortality) was performed on 110 white laboratory mice (BALB / c line). This experimental study was carried out in two replicates. To accomplish this task, the mice were divided into two groups: control – the animals were on a standard diet, and experimental – they used water with the addition of sodium form of bentonite gel (0.5-1%). It was found that prolonged intake of bentonite gel by laboratory animals neither led to an excessive increase in their weight (the weight gain of the experimental group did not differ statistically significantly from the control group, p≤0.05), nor did it cause acute or chronic intoxication. It is also shown that the constant use of bentonite has a positive effect on the organism of experimental mice, which is expressed in the decrease of animal mortality, increase of life expectancy and pronounced positive effect on fertility functions (increase in the number of offspring). Based on the obtained data it can be assumed that the continuous intake of bentonite by the animal organism is one of the factors of their microbiome improvement, which affects on a plenty of physiological functions, including animals reproduction. It is possible that smectite sorbents also enrich the body of mice by certain essential mineral elements (silicon, etc.) and has cytomucoprotective properties concerning the mucous membranes of the macroorganism

Chronic generalized periodontitis as a result of disorders of biotope biofilm of oral cavity

На підставі клінічного спостереження та біохімічного дослідження ротової рідини пацієнтів з хронічним генералізованим пародонтитом доведена клінічна ефективність використання нового виду мультипробіотика групи «Симбітер®»; На основе клинических наблюдений и биохимических исследований ротовой жидкости больных с хроническим генерализованным пародонтитом обоснована эффективность использования нового вида мультипробиотика группы «Симбитер»; It was proved a clinical efficiency of use of multiprobiotic based on clinical observations and biochemical investigations of oral cavity in patients with chronic generalized periodontitis

Magnetism, FeS colloids, and Origins of Life

A number of features of living systems: reversible interactions and weak bonds underlying motor-dynamics; gel-sol transitions; cellular connected fractal organization; asymmetry in interactions and organization; quantum coherent phenomena; to name some, can have a natural accounting via $physical$ interactions, which we therefore seek to incorporate by expanding the horizons of `chemistry-only' approaches to the origins of life. It is suggested that the magnetic 'face' of the minerals from the inorganic world, recognized to have played a pivotal role in initiating Life, may throw light on some of these issues. A magnetic environment in the form of rocks in the Hadean Ocean could have enabled the accretion and therefore an ordered confinement of super-paramagnetic colloids within a structured phase. A moderate H-field can help magnetic nano-particles to not only overcome thermal fluctuations but also harness them. Such controlled dynamics brings in the possibility of accessing quantum effects, which together with frustrations in magnetic ordering and hysteresis (a natural mechanism for a primitive memory) could throw light on the birth of biological information which, as Abel argues, requires a combination of order and complexity. This scenario gains strength from observations of scale-free framboidal forms of the greigite mineral, with a magnetic basis of assembly. And greigite's metabolic potential plays a key role in the mound scenario of Russell and coworkers-an expansion of which is suggested for including magnetism.Comment: 42 pages, 5 figures, to be published in A.R. Memorial volume, Ed Krishnaswami Alladi, Springer 201

DRB1*03:01 Haplotypes: Differential Contribution to Multiple Sclerosis Risk and Specific Association with the Presence of Intrathecal IgM Bands

BACKGROUND: Multiple sclerosis (MS) is a multifactorial disease with a genetic basis. The strongest associations with the disease lie in the Human Leukocyte Antigen (HLA) region. However, except for the DRB1*15:01 allele, the main risk factor associated to MS so far, no consistent effect has been described for any other variant. One example is HLA-DRB1*03:01, with a heterogeneous effect across populations and studies. We postulate that those discrepancies could be due to differences in the diverse haplotypes bearing that allele. Thus, we aimed at studying the association of DRB1*03:01 with MS susceptibility considering this allele globally and stratified by haplotypes. We also evaluated the association with the presence of oligoclonal IgM bands against myelin lipids (OCMB) in cerebrospinal fluid. METHODS: Genotyping of HLA-B, -DRB1 and -DQA1 was performed in 1068 MS patients and 624 ethnically matched healthy controls. One hundred and thirty-nine MS patients were classified according to the presence (M+, 58 patients)/absence (M-, 81 patients) of OCMB. Comparisons between groups (MS patients vs. controls and M+ vs. M-) were performed with the chi-square test or the Fisher exact test. RESULTS: Association of DRB1*03:01 with MS susceptibility was observed but with different haplotypic contribution, being the ancestral haplotype (AH) 18.2 the one causing the highest risk. Comparisons between M+, M- and controls showed that the AH 18.2 was affecting only M+ individuals, conferring a risk similar to that caused by DRB1*15:01. CONCLUSIONS: The diverse DRB1*03:01-containing haplotypes contribute with different risk to MS susceptibility. The AH 18.2 causes the highest risk and affects only to individuals showing OCMB

Achieving Education for Sustainable Development (ESD) in Early Childhood Education Through Critical Reflection in Transformative Learning

The central role of education in creating a more sustainable future has been already recognized by educators and policy-makers alike. This chapter argues that this can only be truly achieved through the efforts of teachers in implementing an “education of a different kind,” a general educational shift that seeks to encompass a converging transformation of the priorities and mindsets of education professionals. In this regard, the professional preparation of teachers, as the leading actors in shaping children’s learning processes, and their continuous professional development are vital considerations for Education for Sustainable Development (ESD) to be successfully achieved. Linking transformative learning and ESD has emerged as a distinct and useful pedagogy because they both support the process of critically examining habits of mind, then revising these habits and acting upon the revised point of view. This study aims to describe and evaluate the potential of transformative learning in innovating mainstream education toward sustainability by focusing on the role of critical reflection in a capacity building research project realized in Turkey. The data was gathered from 24 early childhood educators using a mixed-method research design involving learning diaries, a learning activities survey, and follow-up interviews. This chapter identified content, context, and application method of the in-service training as factors that have contributed to the reflective practices of the participants. In addition, presenting the implications regarding the individual differences in how learners engage in critical reflection practices, this research offers a framework for a content- and process-based approach derived from Mezirow’s conception of critical reflection

Mutations in PNPLA6 are linked to photoreceptor degeneration and various forms of childhood blindness

Blindness due to retinal degeneration affects millions of people worldwide, but many disease-causing mutations remain unknown. PNPLA6 encodes the patatin-like phospholipase domain containing protein 6, also known as neuropathy target esterase (NTE), which is the target of toxic organophosphates that induce human paralysis due to severe axonopathy of large neurons. Mutations in PNPLA6 also cause human spastic paraplegia characterized by motor neuron degeneration. Here we identify PNPLA6 mutations in childhood blindness in seven families with retinal degeneration, including Leber congenital amaurosis and Oliver McFarlane syndrome. PNPLA6 localizes mostly at the inner segment plasma membrane in photo-receptors and mutations in Drosophila PNPLA6 lead to photoreceptor cell death. We also report that lysophosphatidylcholine and lysophosphatidic acid levels are elevated in mutant Drosophila. These findings show a role for PNPLA6 in photoreceptor survival and identify phospholipid metabolism as a potential therapeutic target for some forms of blindness.Foundation Fighting Blindness CanadaCanadian Institutes of Health ResearchNIHCharles University institutional programmesBIOCEV-Biotechnology and Biomedicine Centre of the Academy of Sciences and Charles University, from the European Regional Development FundMinistry of Health of the Czech RepublicGraduate School of Life Sciences (University of Wuerzburg)Government of Canada through Genome CanadaOntario Genomics InstituteGenome QuebecGenome British ColumbiaMcLaughlin CentreCharles Univ Prague, Inst Inherited Metab Disorders, Fac Med 1, Prague 12000 2, Czech RepublicMcGill Univ, Dept Human Genet, Fac Med, Montreal, PQ H3A 0G1, CanadaGenome Quebec Innovat Ctr, Montreal, PQ H3A 0G1, CanadaClin Res Inst Montreal, Cellular Neurobiol Res Unit, Montreal, PQ H2W 1R7, CanadaMcGill Univ, Montreal, PQ H3A 0G4, CanadaMcGill Univ, Ctr Hlth, Montreal Childrens Hosp, McGill Ocular Genet Lab, Montreal, PQ H3H 1P3, CanadaMcGill Univ, Ctr Hlth, Montreal Childrens Hosp, Dept Paediat Surg, Montreal, PQ H3H 1P3, CanadaMcGill Univ, Ctr Hlth, Montreal Childrens Hosp, Dept Human Genet, Montreal, PQ H3H 1P3, CanadaMcGill Univ, Ctr Hlth, Montreal Childrens Hosp, Dept Ophthalmol, Montreal, PQ H3H 1P3, CanadaUniv Alberta, Royal Alexandra Hosp, Dept Ophthalmol & Visual Sci, Edmonton, AB T5H 3V9, CanadaCharles Univ Prague, Inst Biol & Med Genet, Fac Med 1, Prague 12000 2, Czech RepublicBaylor Coll Med, Dept Mol & Human Genet, Human Genome Sequencing Ctr, Houston, TX 77030 USAUniversidade Federal de São Paulo, Dept Neurol, Div Gen Neurol, BR-04021001 São Paulo, BrazilUniversidade Federal de São Paulo, Dept Neurol, Ataxia Unit, BR-04021001 São Paulo, BrazilNewcastle Univ, Inst Med Genet, Newcastle Upon Tyne NE1 3BZ, Tyne & Wear, EnglandUniversidade Federal de São Paulo, Dept Ophthalmol, BR-04021001 São Paulo, BrazilSo Gen Hosp, Dept Clin Genet, Glasgow G51 4TF, Lanark, ScotlandCardiff Univ, Sch Med, Inst Med Genet, Cardiff CF14 4XN, S Glam, WalesHadassah Hebrew Univ Med Ctr, Dept Ophthalmol, IL-91120 Jerusalem, IsraelOregon Hlth & Sci Univ, Oregon Inst Occupat Hlth Sci, Portland, OR 97239 USAUniv Wurzburg, Lehrstuhl Neurobiol & Genet, D-97074 Wurzburg, GermanyUniv Montreal, Dept Med, Montreal, PQ H3T 1P1, CanadaMcGill Univ, Dept Anat & Cell Biol, Div Expt Med, Montreal, PQ H3A 2B2, CanadaUniversidade Federal de São Paulo, Dept Neurol, Div Gen Neurol, BR-04021001 São Paulo, BrazilUniversidade Federal de São Paulo, Dept Neurol, Ataxia Unit, BR-04021001 São Paulo, BrazilUniversidade Federal de São Paulo, Dept Ophthalmol, BR-04021001 São Paulo, BrazilNIH: EY022356-01NIH: EY018571-05NIH: NS047663-09Charles University institutional programmes: PRVOUK-P24/LF1/3Charles University institutional programmes: UNCE 204011Charles University institutional programmes: SVV2013/266504BIOCEV-Biotechnology and Biomedicine Centre of the Academy of Sciences and Charles University, from the European Regional Development Fund: CZ.1.05/1.1.00/02.0109Ministry of Health of the Czech Republic: NT13116-4/2012Ministry of Health of the Czech Republic: NT14015-3/2013Ontario Genomics Institute: OGI-049Web of Scienc