Characterisation of toxic gaseous emissions from industrial solid waste landfills

International audienceIn France, Hazardous Industrial Waste, once stabilized, are buried in specific landfills. As for all polluting activities, these facilities must report to the EPER Register their toxic gaseous emissions, expressed in mass per year, as soon as they exceed threshold limit values. Campaigns were conducted on two different hazardous waste landfills in order to establish if these facilities needed to report to EPER register. Global fluxes of gaseous components were measured by means of an FID (hydrocarbons) and a PID (halocarbons, aromatics and some non-organic compounds). Specific concentrations of aromatic (BTEX) and chlorinated hydrocarbons were also measured. Gaseous emissions were generally very low. Emissions were only detected for young and medium-aged layers, between 1 day and 3 months old. Due to these low emissions, and to the small surfaces involved, the two landfills do not fall under the EPER emission Register

Age, anticoagulants, hypertension and cardiovascular genetic traits predict cranial ischaemic complications in patients with giant cell arteritis

\ua9 Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ on behalf of EULAR.Objectives: This project aimed to determine whether cranial ischaemic complications at the presentation of giant cell arteritis (GCA) were associated with pre-existing cardiovascular (CV) risk factors, CV disease or genetic risk of CV-related traits. Methods: 1946 GCA patients with clinicodemographic data at GCA presentation were included. Associations between pre-existing CV-related traits (including Polygenic Risk Scores (PRS) for CV traits) and cranial ischaemic complications were tested. A model for cranial ischaemic complications was optimised using an elastic net approach. Positional gene mapping of associated PRS was performed to improve biological understanding. Results: In a sample of 1946 GCA patients (median age=71, 68.7% female), 17% had cranial ischaemic complications at presentation. In univariable analyses, 10 variables were associated with complications (likelihood-ratio test p≤0.05). In multivariable analysis, the two variables with the strongest effects, with or without PRS in the model, were anticoagulant therapy (adjusted OR (95% CI)=0.21 (0.05 to 0.62), p=4.95 710-3) and age (adjusted OR (95% CI)=1.60 (0.73 to 3.66), p=2.52 710-3, for ≥80 years versus <60 years). In sensitivity analyses omitting anticoagulant therapy from multivariable analysis, age and hypertension were associated with cranial ischaemic complications at presentation (hypertension: adjusted OR (95% CI)=1.35 (1.03 to 1.75), p=0.03). Positional gene mapping of an associated transient ischaemic attack PRS identified TEK, CD96 and MROH9 loci. Conclusion: Age and hypertension were risk factors for cranial ischaemic complications at GCA presentation, but in this dataset, anticoagulation appeared protective. Positional gene mapping suggested a role for immune and coagulation-related pathways in the pathogenesis of complications. Further studies are needed before implementation in clinical practice

Tissus durs et âge individuel des vertébrés

Des écailles de bar ont été prélevées pour alimenter des études de dynamique des populations. Compte tenu de l'allocation proportionnelle utilisée, la composition en âge de l'échantillon pourrait être utilisée pour estimer celle de la population. Mais la structure démographique ainsi obtenue est biaisée dans le sens d'un rajeunissement du fait de la plus forte probabilité, chez les individus âgés, de rencontrer des écailles régénérées. Il devient alors nécessaire d'utiliser la composition en taille convertie en composition en âge au moyen d'une clé taille-âge. (Résumé d'auteur

The effects of pre-germination treatments and soil media on seed germination and seedling growth of Tamarind (Tamarindus indica (Linn) in Katsina State, Nigeria

Astudy was conducted to investigate theeffects of pre-germination treatments andsoil media on seed germination andseedling growth of Tamarind (Tamarindusindica) in Katsina State, Nigeria.Germination was monitored in the NurserySection of the Federal University Dutsin-Ma, Katsina State, Nigeria. The experimentwas laid in a Completely RandomizedDesign with four replications. Seedlingheight (SH), stem diameter (SD) andnumber of branches (NB) were measuredat two week intervals and analyzed usingAnalysis of Variance. Means wereseparated using Least SignificantDifference (LSD P≤0.05). Mechanicallyscarified seeds (MS), sown in top soil (S1)(S1MS) and seeds treated with 60 %concentrated Tetraoxosulphate (VI) acid(H2SO4) for 10 minutes (A10) and sown inS1 (S1A10), MS sown in S2 (S2MS), seedstreated with A10 and sown in S2 (S2A10),MS sown in top soil plus river sand plusmanure (S3) (S3MS) and seeds treated withA10 and sown in S3 (S3A10) germinated infirst five days after sowing (DAS) whilethose in the control germinated after ninedays. Treatment with A10 resulted in 100 %germination while MS resulted in 97.5 %germination. MS and seeds soaked inH2SO4 for five (5) minutes (A5) had higherSH values of 8.30 cm and 30.81 cmrespectively and NB values of 2.92. A10and MS had SD values of 3.20 cm and 3.20cm respectively. It is concluded that seedstreated with H2SO4 for 10 minutes and MSat the micropyle are the best pregerminationtreatment for breaking T.indica seeds and recommended for seedsowers so in order to achieve regenerationthat can meet various needs of man

Risk loci involved in giant cell arteritis susceptibility: a genome-wide association study

Background Giant cell arteritis is an age-related vasculitis that mainly affects the aorta and its branches in individuals aged 50 years and older. Current options for diagnosis and treatment are scarce, highlighting the need to better understand its underlying pathogenesis. Genome-wide association studies (GWAS) have emerged as a powerful tool for unravelling the pathogenic mechanisms involved in complex diseases. We aimed to characterise the genetic basis of giant cell arteritis by performing the largest GWAS of this vasculitis to date and to assess the functional consequences and clinical implications of identified risk loci. Methods We collected and meta-analysed genomic data from patients with giant cell arteritis and healthy controls of European ancestry from ten cohorts across Europe and North America. Eligible patients required confirmation of giant cell arteritis diagnosis by positive temporal artery biopsy, positive temporal artery doppler ultrasonography, or imaging techniques confirming large-vessel vasculitis. We assessed the functional consequences of loci associated with giant cell arteritis using cell enrichment analysis, fine-mapping, and causal gene prioritisation. We also performed a drug repurposing analysis and developed a polygenic risk score to explore the clinical implications of our findings. Findings We included a total of 3498 patients with giant cell arteritis and 15 550 controls. We identified three novel loci associated with risk of giant cell arteritis. Two loci, MFGE8 (rs8029053; p=4·96 × 10–8; OR 1·19 [95% CI 1·12–1·26]) and VTN (rs704; p=2·75 × 10–9; OR 0·84 [0·79–0·89]), were related to angiogenesis pathways and the third locus, CCDC25 (rs11782624; p=1·28 × 10–8; OR 1·18 [1·12–1·25]), was related to neutrophil extracellular traps (NETs). We also found an association between this vasculitis and HLA region and PLG. Variants associated with giant cell arteritis seemed to fulfil a specific regulatory role in crucial immune cell types. Furthermore, we identified several drugs that could represent promising candidates for treatment of this disease. The polygenic risk score model was able to identify individuals at increased risk of developing giant cell arteritis (90th percentile OR 2·87 [95% CI 2·15–3·82]; p=1·73 × 10–13). Interpretation We have found several additional loci associated with giant cell arteritis, highlighting the crucial role of angiogenesis in disease susceptibility. Our study represents a step forward in the translation of genomic findings to clinical practice in giant cell arteritis, proposing new treatments and a method to measure genetic predisposition to this vasculitis

Risk loci involved in giant cell arteritis susceptibility: a genome-wide association study

Background Giant cell arteritis is an age-related vasculitis that mainly affects the aorta and its branches in individuals aged 50 years and older. Current options for diagnosis and treatment are scarce, highlighting the need to better understand its underlying pathogenesis. Genome-wide association studies (GWAS) have emerged as a powerful tool for unravelling the pathogenic mechanisms involved in complex diseases. We aimed to characterise the genetic basis of giant cell arteritis by performing the largest GWAS of this vasculitis to date and to assess the functional consequences and clinical implications of identified risk loci. Methods We collected and meta-analysed genomic data from patients with giant cell arteritis and healthy controls of European ancestry from ten cohorts across Europe and North America. Eligible patients required confirmation of giant cell arteritis diagnosis by positive temporal artery biopsy, positive temporal artery doppler ultrasonography, or imaging techniques confirming large-vessel vasculitis. We assessed the functional consequences of loci associated with giant cell arteritis using cell enrichment analysis, fine-mapping, and causal gene prioritisation. We also performed a drug repurposing analysis and developed a polygenic risk score to explore the clinical implications of our findings. Findings We included a total of 3498 patients with giant cell arteritis and 15 550 controls. We identified three novel loci associated with risk of giant cell arteritis. Two loci, MFGE8 (rs8029053; p=4·96 × 10–8; OR 1·19 [95% CI 1·12–1·26]) and VTN (rs704; p=2·75 × 10–9; OR 0·84 [0·79–0·89]), were related to angiogenesis pathways and the third locus, CCDC25 (rs11782624; p=1·28 × 10–8; OR 1·18 [1·12–1·25]), was related to neutrophil extracellular traps (NETs). We also found an association between this vasculitis and HLA region and PLG. Variants associated with giant cell arteritis seemed to fulfil a specific regulatory role in crucial immune cell types. Furthermore, we identified several drugs that could represent promising candidates for treatment of this disease. The polygenic risk score model was able to identify individuals at increased risk of developing giant cell arteritis (90th percentile OR 2·87 [95% CI 2·15–3·82]; p=1·73 × 10–13). Interpretation We have found several additional loci associated with giant cell arteritis, highlighting the crucial role of angiogenesis in disease susceptibility. Our study represents a step forward in the translation of genomic findings to clinical practice in giant cell arteritis, proposing new treatments and a method to measure genetic predisposition to this vasculitis