Methylmercury exposure and developmental neurotoxicity.

Comment on: Global methylmercury exposure from seafood consumption and risk of developmental neurotoxicity: a systematic review. [Bull World Health Organ. 2014]]]> Humans; Methylmercury Compounds; Neurotoxicity Syndromes eng https://serval.unil.ch/resource/serval:BIB_B254C52AD78C.P001/REF.pdf http://nbn-resolving.org/urn/resolver.pl?urn=urn:nbn:ch:serval-BIB_B254C52AD78C2 info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_B254C52AD78C2 info:eu-repo/semantics/publishedVersion info:eu-repo/semantics/openAccess Copying allowed only for non-profit organizations https://serval.unil.ch/disclaimer application/pdf oai:serval.unil.ch:BIB_B254CA78ED67 2022-05-07T01:25:17Z openaire documents urnserval <oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"> https://serval.unil.ch/notice/serval:BIB_B254CA78ED67 Application of a computationally efficient method to approximate gap model results with a probabilistic approach info:doi:10.5194/gmd-7-1543-2014 info:eu-repo/semantics/altIdentifier/doi/10.5194/gmd-7-1543-2014 Scherstjanoi, M. Kaplan, J. O. Lischke, H. info:eu-repo/semantics/article article 2014 Geoscientific Model Development, vol. 7, no. 4, pp. 1543-1571 urn:issn:1991-959x eng https://serval.unil.ch/resource/serval:BIB_B254CA78ED67.P001/REF.pdf http://nbn-resolving.org/urn/resolver.pl?urn=urn:nbn:ch:serval-BIB_B254CA78ED677 info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_B254CA78ED677 info:eu-repo/semantics/publishedVersion info:eu-repo/semantics/openAccess Copying allowed only for non-profit organizations https://serval.unil.ch/disclaimer application/pdf oai:serval.unil.ch:BIB_B254D0E85D5E 2022-05-07T01:25:17Z <oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"> https://serval.unil.ch/notice/serval:BIB_B254D0E85D5E Meningite purulente aigue a Listeria seeligeri chez un adulte immunocompetent. [Acute purulent Listeria seelingeri meningitis in an immunocompetent adult] info:eu-repo/semantics/altIdentifier/pmid/3082004 Rocourt, J. Hof, H. Schrettenbrunner, A. Malinverni, R. Bille, J. info:eu-repo/semantics/article article 1986-02 Schweizerische Medizinische Wochenschrift, vol. 116, no. 8, pp. 248-51 info:eu-repo/semantics/altIdentifier/pissn/0036-7672 <![CDATA[Within the genus Listeria, the species L. monocytogenes most frequently causes disease in animals and humans. L. Seeligeri, a species recently described, has been considered experimentally nonpathogenic so far. The authors report the first case of human infection in a previously healthy adult presenting with acute purulent meningitis due to L. seeligeri. The patient recovered promptly after a course of ampicillin and gentamicin, but developed severe neurological sequelae (epilepsy, hydrocephalus) one year after the acute episode. The pathogenic properties of this isolate were investigated in two experimental animal models and the results were as follows. The clinical isolate of L. seeligeri was able to colonize the spleens of adult mice without bacterial multiplication, in contrast to the type strain of L. seeligeri (no colonization) and to a L. monocytogenes strain (colonization and multiplication). Previous infection of adult mice with the clinical L. seeligeri isolate protected moderately against spleen colonization and bacterial multiplication after challenge with L. monocytogenes. No lethal effect was observed after inoculation of suckling mice with the clinical L. seeligeri isolate, in contrast to L. monocytogenes strains. Thus, L. seeligeri, previously described as experimentally nonpathogenic for mice, may in fact be a heterogeneous species regarding its pathogenicity, and include strains that may cause life-threatening diseases in humans

Asymptotic Stability of the Relativistic Boltzmann Equation for the Soft Potentials

In this paper it is shown that unique solutions to the relativistic Boltzmann equation exist for all time and decay with any polynomial rate towards their steady state relativistic Maxwellian provided that the initial data starts out sufficiently close in $L^\infty_\ell$. If the initial data are continuous then so is the corresponding solution. We work in the case of a spatially periodic box. Conditions on the collision kernel are generic in the sense of (Dudy{\'n}ski and Ekiel-Je{\.z}ewska, Comm. Math. Phys., 1988); this resolves the open question of global existence for the soft potentials.Comment: 64 page

Impact of the MTHFR C677T polymorphism on one-carbon metabolites: Evidence from a randomised trial of riboflavin supplementation

Homozygosity for the C677T polymorphism in MTHFR (TT genotype) is associated with a 24–87% increased risk of hypertension. Blood pressure (BP) lowering was previously reported in adults with the TT genotype, in response to supplementation with the MTHFR cofactor, riboflavin. Whether the BP phenotype associated with the polymorphism is related to perturbed one-carbon metabolism is unknown. This study investigated one-carbon metabolites and their responsiveness to riboflavin in adults with the TT genotype. Plasma samples from adults (n 115) screened for the MTHFR genotype, who previously participated in RCTs to lower BP, were analysed for methionine, S-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH), betaine, choline and cystathionine by liquid chromatography tandem mass spectrometry (LC-MS/MS). The one-carbon metabolite response to riboflavin (1.6 mg/d; n 24) or placebo (n 23) for 16 weeks in adults with the TT genotype was also investigated. Plasma SAM (74.7 ± 21.0 vs 85.2 ± 22.6 nmol/L, P = 0.013) and SAM:SAH ratio (1.66 ± 0.55 vs 1.85 ± 0.51, P = 0.043) were lower and plasma homocysteine was higher (P = 0.043) in TT, compared to CC individuals. In response to riboflavin, SAM (P = 0.008) and cystathionine (P = 0.045) concentrations increased, with no responses in other one-carbon metabolites observed. These findings confirm perturbed one-carbon metabolism in individuals with the MTHFR 677TT genotype, and for the first time demonstrate that SAM, and cystathionine, increase in response to riboflavin supplementation in this genotype group. The genotype-specific, one-carbon metabolite responses to riboflavin intervention observed could offer some insight into the role of this gene-nutrient interaction in blood pressure

The Reduced Folate Carrier (SLC19A1) c.80G&gt;A Polymorphism is associated with red cell folate concentrations among women

Low folate status may be a consequence of suboptimal intake, transport or cellular utilization of folate and, together with elevated homocysteine, is a recognized risk factor/marker for several human pathologies. As folate transport across cell membranes is mediated in part by the reduced folate carrier (RFC1), variants within this gene may influence disease risk via an effect on folate and/or homocysteine levels. The present study was undertaken to assess the association between the SLC19A1 (RFC1) c.80G>A polymorphism and folate/homocysteine concentrations in healthy young adults from Northern Ireland. The SLC19A1 c.80G>A polymorphism was not strongly associated with either serum folate or homocysteine concentrations in either men or women. However, in women, but not in men, this polymorphism explained 5% of the variation in red blood cell (RBC) folate levels (P=0.02). Relative to women with the SLC19A1 c.80GG genotype, women with the GA and AA genotypes had higher RBC folate concentrations. Consequently, compared to women with the SLC19A1 c.80AA and GA genotypes, women who are homozygous for the 80G allele may be at increased risk of having a child affected with a neural tube defect and of developing pathologies that have been associated with folate insufficiency, such as cardiovascular disease

Prenatal methylmercury exposure and DNA methylation in seven-year-old children in the Seychelles Child Development Study

Background Methylmercury (MeHg) is present in fish and is a neurotoxicant at sufficiently high levels. One potential mechanism of MeHg toxicity early in life is epigenetic dysregulation that may affect long-term neurodevelopment. Altered DNA methylation of nervous system-related genes has been associated with adult mental health outcomes. Objective To assess associations between prenatal MeHg exposure and DNA methylation (at the cytosine of CG dinucleotides, CpGs) in three nervous system-related genes, encoding brain-derived neurotropic factor (BDNF), glutamate receptor subunit NR2B (GRIN2B), and the glucocorticoid receptor (NR3C1), in children who were exposed to MeHg in utero. Methods We tested 406 seven-year-old Seychellois children participating in the Seychelles Child Development Study (Nutrition Cohort 2), who were prenatally exposed to MeHg from maternal fish consumption. Total mercury in maternal hair (prenatal MeHg exposure measure) collected during pregnancy was measured using atomic absorption spectroscopy. Methylation in DNA from the children’s saliva was measured by pyrosequencing. To assess associations between prenatal MeHg exposure and CpG methylation at seven years of age, we used multivariable linear regression models adjusted for covariates. Results We identified associations with prenatal MeHg exposure for DNA methylation of one GRIN2B CpG and two NR3C1 CpGs out of 12 total CpG sites. Higher prenatal MeHg was associated with higher methylation for each CpG site. For example, NR3C1 CpG3 had an expected increase of 0.03-fold for each additional 1 ppm of prenatal MeHg (B = 0.030, 95% CI 0.001, 0.059; p = 0.047). Several CpG sites associated with MeHg are located in transcription factor binding sites and the observed methylation changes are predicted to lead to lower gene expression. Conclusions In a population of people who consume large amounts of fish, we showed that higher prenatal MeHg exposure was associated with differential DNA methylation at seven years of age at specific CpG sites that may influence neurodevelopment and mental health

The Effect of Processing and Seasonallity on the Iodine and Selenium Concentration of Cow's Milk Produced in Northern Ireland (NI): Implications for Population Dietary Intake

Cow’s milk is the most important dietary source of iodine in the UK and Ireland, and also contributes to dietary selenium intakes. The aim of this study was to investigate the effect of season, milk fat class (whole; semi-skimmed; skimmed) and pasteurisation on iodine and selenium concentrations in Northern Ireland (NI) milk, and to estimate the contribution of this milk to consumer iodine and selenium intakes. Milk samples (unpasteurised, whole, semi-skimmed and skimmed) were collected weekly from two large NI creameries between May 2013 and April 2014 and were analysed by inductively coupled plasma-mass spectrometry (ICP-MS). Using milk consumption data from the National Diet and Nutrition Survey (NDNS) Rolling Programme, the contribution of milk (at iodine and selenium concentrations measured in the present study) to UK dietary intakes was estimated. The mean ± standard deviation (SD) iodine concentration of milk was 475.9 ± 63.5 µg/kg and the mean selenium concentration of milk was 17.8 ± 2.7 µg/kg. Season had an important determining effect on the iodine, but not the selenium, content of cow’s milk, where iodine concentrations were highest in milk produced in spring compared to autumn months (534.3 ± 53.7 vs. 433.6 ± 57.8 µg/kg, respectively; p = 0.001). The measured iodine and selenium concentrations of NI milk were higher than those listed in current UK Food Composition Databases (Food Standards Agency (FSA) (2002); FSA (2015)). The dietary modelling analysis confirmed that milk makes an important contribution to iodine and selenium intakes. This contribution may be higher than previously estimated if iodine and selenium (+25.0 and +1.1 µg/day respectively) concentrations measured in the present study were replicable across the UK at the current level of milk consumption. Iodine intakes were theoretically shown to vary by season concurrent with the seasonal variation in NI milk iodine concentrations. Routine monitoring of milk iodine concentrations is required and efforts should be made to understand reasons for fluctuations in milk iodine concentrations, in order to realise the nutritional impact to consumers