SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "WFRF:(Lucena R.) "

Sökning: WFRF:(Lucena R.)

  • Resultat 1-18 av 18
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
1.
  •  
2.
  •  
3.
  • Formiga-Cruz, M, et al. (författare)
  • Evaluation of potential indicators of viral contamination in shellfish and their applicability to diverse geographical areas.
  • 2003
  • Ingår i: Applied and Environmental Microbiology. - 0099-2240 .- 1098-5336. ; 69:3, s. 1556-63
  • Tidskriftsartikel (refereegranskat)abstract
    • The distribution of the concentration of potential indicators of fecal viral pollution in shellfish was analyzed under diverse conditions over 18 months in diverse geographical areas. These microorganisms have been evaluated in relation to contamination by human viral pathogens detected in parallel in the analyzed shellfish samples. Thus, significant shellfish-growing areas from diverse countries in the north and south of Europe (Greece, Spain, Sweden, and the United Kingdom) were defined and studied by analyzing different physicochemical parameters in the water and the levels of Escherichia coli, F-specific RNA bacteriophages, and phages infecting Bacteroides fragilis strain RYC2056 in the shellfish produced, before and after depuration treatments. A total of 475 shellfish samples were studied, and the results were statistically analyzed. According to statistical analysis, the presence of human viruses seems to be related to the presence of all potential indicators in the heavily contaminated areas, where E. coli would probably be suitable as a fecal indicator. The F-RNA phages, which are present in higher numbers in Northern Europe, seem to be significantly related to the presence of viral contamination in shellfish, with a very weak predictive value for hepatitis A virus, human adenovirus, and enterovirus and a stronger one for Norwalk-like virus. However, it is important to note that shellfish produced in A or clean B areas can sporadically contain human viruses even in the absence of E. coli or F-RNA phages. The data presented here will be useful in defining microbiological parameters for improving the sanitary control of shellfish consumed raw or barely cooked.
  •  
4.
  • Formiga-Cruz, M, et al. (författare)
  • Evaluation of potential indicators of viral contamination in shellfish and their applicability to diverse geographical areas
  • 2003
  • Ingår i: Applied and Environmental Microbiology. - 0099-2240 .- 1098-5336. ; 69:3, s. 1556-1563
  • Tidskriftsartikel (refereegranskat)abstract
    • The distribution of the concentration of potential indicators of fecal viral pollution in shellfish was analyzed under diverse conditions over 18 months in diverse geographical areas. These microorganisms have been evaluated in relation to contamination by human viral pathogens detected in parallel in the analyzed shellfish samples. Thus, significant shellfish-growing areas from diverse countries in the north and south of Europe (Greece, Spain, Sweden, and the United Kingdom) were defined and studied by analyzing different physicochemical parameters in the water and the levels of Escherichia coli, F-specific RNA bacteriophages, and phages infecting Bacteroides fragilis strain RYC2056 in the shellfish produced, before and after depuration treatments. A total of 475 shellfish samples were studied, and the results were statistically analyzed. According to statistical analysis, the presence of human viruses seems to be related to the presence of all potential indicators in the heavily contaminated areas, where E. coli would probably be suitable as a fecal indicator. The F-RNA phages, which are present in higher numbers in Northern Europe, seem to be significantly related to the presence of viral contamination in shellfish, with a very weak predictive value for hepatitis A virus, human adenovirus, and enterovirus and a stronger one for Norwalk-like virus. However, it is important to note that shellfish produced in A or clean B areas can sporadically contain human viruses even in the absence of E. coli or F-RNA phages. The data presented here will be useful in defining microbiological parameters for improving the sanitary control of shellfish consumed raw or barely cooked.
  •  
5.
  • Marhold, Karol, et al. (författare)
  • IAPT chromosome data 39-Extended version
  • 2023
  • Ingår i: Taxon. - : John Wiley & Sons. - 0040-0262 .- 1996-8175. ; 72:5, s. 1189-1192
  • Tidskriftsartikel (refereegranskat)
  •  
6.
  • Oikonomou, Vasileios, et al. (författare)
  • The Role of Interferon-γ in Autoimmune Polyendocrine Syndrome Type 1.
  • 2024
  • Ingår i: The New England journal of medicine. - 1533-4406. ; 390:20, s. 1873-1884
  • Tidskriftsartikel (refereegranskat)abstract
    • Autoimmune polyendocrine syndrome type 1 (APS-1) is a life-threatening, autosomal recessive syndrome caused by autoimmune regulator (AIRE) deficiency. In APS-1, self-reactive T cells escape thymic negative selection, infiltrate organs, and drive autoimmune injury. The effector mechanisms governing T-cell-mediated damage in APS-1 remain poorly understood.We examined whether APS-1 could be classified as a disease mediated by interferon-γ. We first assessed patients with APS-1 who were participating in a prospective natural history study and evaluated mRNA and protein expression in blood and tissues. We then examined the pathogenic role of interferon-γ using Aire-/-Ifng-/- mice and Aire-/- mice treated with the Janus kinase (JAK) inhibitor ruxolitinib. On the basis of our findings, we used ruxolitinib to treat five patients with APS-1 and assessed clinical, immunologic, histologic, transcriptional, and autoantibody responses.Patients with APS-1 had enhanced interferon-γ responses in blood and in all examined autoimmunity-affected tissues. Aire-/- mice had selectively increased interferon-γ production by T cells and enhanced interferon-γ, phosphorylated signal transducer and activator of transcription 1 (pSTAT1), and CXCL9 signals in multiple organs. Ifng ablation or ruxolitinib-induced JAK-STAT blockade in Aire-/- mice normalized interferon-γ responses and averted T-cell infiltration and damage in organs. Ruxolitinib treatment of five patients with APS-1 led to decreased levels of T-cell-derived interferon-γ, normalized interferon-γ and CXCL9 levels, and remission of alopecia, oral candidiasis, nail dystrophy, gastritis, enteritis, arthritis, Sjögren's-like syndrome, urticaria, and thyroiditis. No serious adverse effects from ruxolitinib were identified in these patients.Our findings indicate that APS-1, which is caused by AIRE deficiency, is characterized by excessive, multiorgan interferon-γ-mediated responses. JAK inhibition with ruxolitinib in five patients showed promising results. (Funded by the National Institute of Allergy and Infectious Diseases and others.).
  •  
7.
  • Abdel-Rehim, Mohamed, et al. (författare)
  • Microextraction approaches for bioanalytical applications : An overview
  • 2020
  • Ingår i: Journal of Chromatography A. - : Elsevier B.V.. - 0021-9673 .- 1873-3778. ; 1616
  • Tidskriftsartikel (refereegranskat)abstract
    • Biological samples are usually complex matrices due to the presence of proteins, salts and a variety of organic compounds with chemical properties similar to those of the target analytes. Therefore, sample preparation is often mandatory in order to isolate the analytes from troublesome matrices before instrumental analysis. Because the number of samples in drug development, doping analysis, forensic science, toxicological analysis, and preclinical and clinical assays is steadily increasing, novel high throughput sample preparation approaches are calling for. The key factors in this development are the miniaturization and the automation of the sample preparation approaches so as to cope with most of the twelve principles of green chemistry. In this review, recent trends in sample preparation and novel strategies will be discussed in detail with particular focus on sorptive and liquid-phase microextraction in bioanalysis. The actual applicability of selective sorbents is also considered. Additionally, the role of 3D printing in microextraction for bioanalytical methods will be pinpointed.
  •  
8.
  • Arahal, David R., et al. (författare)
  • Marinomonas blandensis sp nova, a novel marine gammaproteobacterium
  • 2016
  • Ingår i: International Journal of Systematic and Evolutionary Microbiology. - : Microbiology Society. - 1466-5026 .- 1466-5034. ; 66, s. 5544-5549
  • Tidskriftsartikel (refereegranskat)abstract
    • A novel Gram-staining-negative, chemoorganotrophic, moderately halophilic, strictly aerobic bacterium, strain MED121(T), was isolated from a seawater sample collected at the Blanes Bay Microbial Observatory in the north-western Mediterranean Sea. Analysis of its 16S rRNA gene sequence, retrieved from the whole-genome sequence, showed that this bacterium was most closely related to Marinomonas dokdonensis and other Marinomonas species (96.3 and 93.3-95.7% sequence similarities, respectively), within the family Oceanospirillaceae. Strain MED121(T) was included into a whole-genome sequencing study and, subsequently, it was characterized using a polyphasic taxonomic approach. It was found to be oxidase and catalase positive, its cells are cocci to short rods, it does not ferment carbohydrates and does not reduce nitrate to nitrite or gas and it requires at least 2.5% (w/v) marine salts and tolerates up to 7% (w/v) salts. Its major cellular fatty acids in order of abundance are C-16:1 omega 7c/C-16:1 omega 6c,C-18:1 omega 7c(1), C-16:0 and C-10:0 3-OH. Its genome had an approximate length of 5.1 million bases and a DNA G+C content equal to 40.9 mol%. Analysis of the annotated genes reveals the capacity for the synthesis of ubiquinone 8 (O8) and the polar lipids phosphatidylglycerol and phosphatidylethanolannine, in agreement with other members of the genus. All the data collected supported the creation of a novel species to accommodate this bacterium, for which the name Marinomonas blandensis sp. nov. is proposed. The type strain is MED121(T) (=CECT 7076(T)=LMG 29722(T)).
  •  
9.
  • Cirulli, Elizabeth T., et al. (författare)
  • A Missense Variant in PTPN22 is a Risk Factor for Drug-induced Liver Injury
  • 2019
  • Ingår i: Gastroenterology. - : W B SAUNDERS CO-ELSEVIER INC. - 0016-5085 .- 1528-0012. ; 156:6, s. 1707-1716
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND & AIMS: We performed genetic analyses of a multiethnic cohort of patients with idiosyncratic drug-induced liver injury (DILI) to identify variants associated with susceptibility.METHODS: We performed a genome-wide association study of 2048 individuals with DILI (cases) and 12,429 individuals without (controls). Our analysis included subjects of European (1806 cases and 10,397 controls), African American (133 cases and 1,314 controls), and Hispanic (109 cases and 718 controls) ancestry. We analyzed DNA from 113 Icelandic cases and 239,304 controls to validate our findings.RESULTS: We associated idiosyncratic DILI with rs2476601, a nonsynonymous polymorphism that encodes a substitution of tryptophan with arginine in the protein tyrosine phosphatase, nonreceptor type 22 gene (PTPN22) (odds ratio [OR] 1.44; 95% confidence interval [CI] 1.28-1.62; P = 1.2 x 10(-9) and replicated the finding in the validation set (OR 1.48; 95% CI 1.09-1.99; P =.01). The minor allele frequency showed the same effect size (OR > 1) among ethnic groups. The strongest association was with amoxicillin and clavulanate-associated DILI in persons of European ancestry (OR 1.62; 95% CI 1.32-1.98; P = 4.0 x 10(-6); allele frequency = 13.3%), but the polymorphism was associated with DILI of other causes (OR 1.37; 95% CI 1.21-1.56; P = 1.5 x 10(-6); allele frequency = 11.5%). Among amoxicillin-and clavulanate-associated cases of European ancestry, rs2476601 doubled the risk for DILI among those with the HLA risk alleles A* 02: 01 and DRB1* 15: 01.CONCLUSIONS: In a genome-wide association study, we identified rs2476601 in PTPN22 as a non-HLA variant that associates with risk of liver injury caused by multiple drugs and validated our finding in a separate cohort. This variant has been associated with increased risk of autoimmune diseases, providing support for the concept that alterations in immune regulation contribute to idiosyncratic DILI.
  •  
10.
  • Cismaru, Anca Liliana, et al. (författare)
  • Genome-Wide Association Study of Metamizole-Induced Agranulocytosis in European Populations
  • 2020
  • Ingår i: Genes. - : MDPI AG. - 2073-4425. ; 11:11
  • Tidskriftsartikel (refereegranskat)abstract
    • Agranulocytosis is a rare yet severe idiosyncratic adverse drug reaction to metamizole, an analgesic widely used in countries such as Switzerland and Germany. Notably, an underlying mechanism has not yet been fully elucidated and no predictive factors are known to identify at-risk patients. With the aim to identify genetic susceptibility variants to metamizole-induced agranulocytosis (MIA) and neutropenia (MIN), we conducted a retrospective multi-center collaboration including cases and controls from three European populations. Association analyses were performed using genome-wide genotyping data from a Swiss cohort (45 cases, 191 controls) followed by replication in two independent European cohorts (41 cases, 273 controls) and a joint discovery meta-analysis. No genome-wide significant associations (p < 1 × 10−7) were observed in the Swiss cohort or in the joint meta-analysis, and no candidate genes suggesting an immune-mediated mechanism were identified. In the joint meta-analysis of MIA cases across all cohorts, two candidate loci on chromosome 9 were identified, rs55898176 (OR = 4.01, 95%CI: 2.41–6.68, p = 1.01 × 10−7) and rs4427239 (OR = 5.47, 95%CI: 2.81–10.65, p = 5.75 × 10−7), of which the latter is located in the SVEP1 gene previously implicated in hematopoiesis. This first genome-wide association study for MIA identified suggestive associations with biological plausibility that may be used as a stepping-stone for post-GWAS analyses to gain further insight into the mechanism underlying MIA.
  •  
11.
  • Diaz-Lucena, D., et al. (författare)
  • TREM2 expression in the brain and biological fluids in prion diseases
  • 2021
  • Ingår i: Acta Neuropathologica. - : Springer Science and Business Media LLC. - 0001-6322 .- 1432-0533. ; 141, s. 841-859
  • Tidskriftsartikel (refereegranskat)abstract
    • Triggering receptor expressed on myeloid cells 2 (TREM2) is an innate immune cell surface receptor that regulates microglial function and is involved in the pathophysiology of several neurodegenerative diseases. Its soluble form (sTREM2) results from shedding of the TREM2 ectodomain. The role of TREM2 in prion diseases, a group of rapidly progressive dementias remains to be elucidated. In the present study, we analysed the expression of TREM2 and its main sheddase ADAM10 in the brain of sporadic Creutzfeldt-Jakob disease (sCJD) patients and evaluated the role of CSF and plasma sTREM2 as a potential diagnostic marker of prion disease. Our data indicate that, compared to controls, TREM2 is increased in sCJD patient brains at the mRNA and protein levels in a regional and subtype dependent fashion, and expressed in a subpopulation of microglia. In contrast, ADAM10 is increased at the protein, but not the mRNA level, with a restricted neuronal expression. Elevated CSF sTREM2 is found in sCJD, genetic CJD with mutations E200K and V210I in the prion protein gene (PRNP), and iatrogenic CJD, as compared to healthy controls (HC) (AUC = 0.78-0.90) and neurological controls (AUC = 0.73-0.85), while CSF sTREM2 is unchanged in fatal familial insomnia. sTREM2 in the CSF of cases with Alzheimer's disease, and multiple sclerosis was not significantly altered in our series. CSF sTREM2 concentrations in sCJD are PRNP codon 129 and subtype-related, correlate with CSF 14-3-3 positivity, total-tau and YKL-40, and increase with disease progression. In plasma, sTREM2 is increased in sCJD compared with HC (AUC = 0.80), displaying positive correlations with plasma total-tau, neurofilament light, and YKL-40. We conclude that comparative study of TREM2 in brain and biological fluids of prion diseases reveals TREM2 to be altered in human prion diseases with a potential value in target engagement, patient stratification, and disease monitoring.
  •  
12.
  • Mikus, Maria, et al. (författare)
  • Elevated levels of circulating CDH5 and FABP1 in association with human drug-induced liver injury
  • 2016
  • Ingår i: Liver international. - : John Wiley & Sons. - 1478-3223 .- 1478-3231. ; 37:1, s. 132-140
  • Tidskriftsartikel (refereegranskat)abstract
    • Background & Aims: The occurrence of drug-induced liver injury (DILI) is a major issue in all phases of drug development. To identify novel biomarker candidates associated with DILI, we utilised an affinity proteomics strategy, where antibody suspension bead arrays were applied to profile plasma and serum samples from human DILI cases and controls. Methods: An initial screening was performed using 4594 randomly selected antibodies, representing 3450 human proteins. Resulting candidate proteins together with proposed DILI biomarker candidates generated a DILI array of 251 proteins for subsequent target analysis and verifications. In total, 1196 samples from 241 individuals across four independent cohorts were profiled: healthy volunteers receiving acetaminophen, patients with human immunodeficiency virus and/or tuberculosis receiving treatment, DILI cases originating from a wide spectrum of drugs, and healthy volunteers receiving heparins. Results: We observed elevated levels of cadherin 5, type 2 (CDH5) and fatty acid-binding protein 1 (FABP1) in DILI cases. In the two longitudinal cohorts, CDH5 was elevated already at baseline. FABP1 was elevated after treatment initiation and seemed to respond more rapidly than alanine aminotransferase (ALT). The elevations were verified in the DILI cases treated with various drugs. In the heparin cohort, CDH5 was stable over time whereas FABP1 was elevated. Conclusions: These results suggest that CDH5 may have value as a susceptibility marker for DILI. FABP1 was identified as a biomarker candidate with superior characteristics regarding tissue distribution and kinetics compared to ALT but likely with limited predictive value for the development of severe DILI. Further studies are needed to determine the clinical utility of the proposed markers.
  •  
13.
  • Nicoletti, Paola, et al. (författare)
  • Association of Liver Injury From Specific Drugs, or Groups of Drugs, With Polymorphisms in HLA and Other Genes in a Genome-Wide Association Study
  • 2017
  • Ingår i: Gastroenterology. - : W B SAUNDERS CO-ELSEVIER INC. - 0016-5085 .- 1528-0012. ; 152:5, s. 1078-1089
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND & AIMS: We performed a genome-wide association study (GWAS) to identify genetic risk factors for druginduced liver injury (DILI) from licensed drugs without previously reported genetic risk factors. METHODS: We performed a GWAS of 862 persons with DILI and 10,588 population-matched controls. The first set of cases was recruited before May 2009 in Europe (n = 137) and the United States (n = 274). The second set of cases were identified from May 2009 through May 2013 from international collaborative studies performed in Europe, the United States, and South America. For the GWAS, we included only cases with patients of European ancestry associated with a particular drug (but not flucloxacillin or amoxicillin-clavulanate). We used DNA samples from all subjects to analyze HLA genes and single nucleotide polymorphisms. After the discovery analysis was concluded, we validated our findings using data from 283 European patients with diagnosis of DILI associated with various drugs. RESULTS: We associated DILI with rs114577328 (a proxy for A* 33: 01 a HLA class I allele; odds ratio [OR], 2.7; 95% confidence interval [CI], 1.9 - 3.8; P = 2.4 x 10(-8)) and with rs72631567 on chromosome 2 (OR, 2.0; 95% CI, 1.6 - 2.5; P = 9.7 x 10(-9)). The association with A* 33: 01 was mediated by large effects for terbinafine-, fenofibrate-, and ticlopidine-related DILI. The variant on chromosome 2 was associated with DILI from a variety of drugs. Further phenotypic analysis indicated that the association between DILI and A* 33: 01 was significant genome wide for cholestatic and mixed DILI, but not for hepatocellular DILI; the polymorphism on chromosome 2 was associated with cholestatic and mixed DILI as well as hepatocellular DILI. We identified an association between rs28521457 (within the lipopolysaccharide-responsive vesicle trafficking, beach and anchor containing gene) and only hepatocellular DILI (OR, 2.1; 95% CI, 1.6 - 2.7; P = 4.8 x 10(-9)). We did not associate any specific drug classes with genetic polymorphisms, except for statin-associated DILI, which was associated with rs116561224 on chromosome 18 (OR, 5.4; 95% CI, 3.0 - 9.5; P = 7.1 x 10(-9)). We validated the association between A* 33: 01 terbinafine-and sertraline-induced DILI. We could not validate the association between DILI and rs72631567, rs28521457, or rs116561224. CONCLUSIONS: In a GWAS of persons of European descent with DILI, we associated HLA-A* 33: 01 with DILI due to terbinafine and possibly fenofibrate and ticlopidine. We identified polymorphisms that appear to be associated with DILI from statins, as well as 2 non-drug-specific risk factors.
  •  
14.
  • Nicoletti, Paola, et al. (författare)
  • Drug-Induced Liver Injury due to Flucloxacillin : Relevance of Multiple Human Leukocyte Antigen Alleles
  • 2019
  • Ingår i: Clinical Pharmacology and Therapeutics. - : John Wiley & Sons. - 0009-9236 .- 1532-6535. ; 106:1, s. 245-253
  • Tidskriftsartikel (refereegranskat)abstract
    • Some patients prescribed flucloxacillin (similar to 0.01%) develop drug-induced liver injury (DILI). HLA-B*57:01 is an established genetic risk factor for flucloxacillin DILI. To consolidate this finding, identify additional genetic factors, and assess relevance of risk factors for flucloxacillin DILI in relation to DILI due to other penicillins, we performed a genomewide association study involving 197 flucloxacillin DILI cases and 6,835 controls. We imputed single-nucleotide polymorphism and human leukocyte antigen (HLA) genotypes. HLA-B*57:01 was the major risk factor (allelic odds ratio (OR) = 36.62; P = 2.67 x 10(-97)). HLA-B*57:03 also showed an association (OR = 79.21; P = 1.2 x 10(-6)). Within the HLA-B protein sequence, imputation showed valine(97), common to HLA-B*57:01 and HLA-B*57:03, had the largest effect (OR = 38.1; P = 9.7 x 10(-97)). We found no HLA-B*57 association with DILI due to other isoxazolyl penicillins (n = 6) or amoxicillin (n = 15) and no significant non-HLA signals for any penicillin-related DILI.
  •  
15.
  • Nicoletti, Paola, et al. (författare)
  • Shared Genetic Risk Factors Across Carbamazepine-Induced Hypersensitivity Reactions
  • 2019
  • Ingår i: Clinical Pharmacology and Therapeutics. - : John Wiley & Sons. - 0009-9236 .- 1532-6535. ; 106:5, s. 1028-1036
  • Tidskriftsartikel (refereegranskat)abstract
    • Carbamazepine (CBZ) causes life-threating T-cell-mediated hypersensitivity reactions, including serious cutaneous adverse reactions (SCARs) and drug-induced liver injury (CBZ-DILI). In order to evaluate shared or phenotype-specific genetic predisposing factors for CBZ hypersensitivity reactions, we performed a meta-analysis of two genomewide association studies (GWAS) on a total of 43 well-phenotyped Northern and Southern European CBZ-SCAR cases and 10,701 population controls and a GWAS on 12 CBZ-DILI cases and 8,438 ethnically matched population controls. HLA-A*31:01 was identified as the strongest genetic predisposing factor for both CBZ-SCAR (odds ratio (OR) = 8.0; 95% CI 4.10-15.80; P = 1.2 x 10(-9)) and CBZ-DILI (OR = 7.3; 95% CI 2.47-23.67; P = 0.0004) in European populations. The association with HLA-A*31:01 in patients with SCAR was mainly driven by hypersensitivity syndrome (OR = 12.9; P = 2.1 x 10(-9)) rather than by Stevens-Johnson syndrome/toxic epidermal necrolysis cases, which showed an association with HLA-B*57:01. We also identified a novel risk locus mapping to ALK only for CBZ-SCAR cases, which needs replication in additional cohorts and functional evaluation.
  •  
16.
  •  
17.
  • Palacios, M.A., et al. (författare)
  • Platinum-group elements: quantification in collected exhaust fumes and studies of catalyst surfaces
  • 2000
  • Ingår i: The Science of the Total Environment. ; 257, s. 1-15
  • Tidskriftsartikel (refereegranskat)abstract
    • Automotive catalytic converters, in which Pt, Pd and Rh (platinum-group elements; PGEs) are the active components for eliminating several noxious components from exhaust fumes, have become the main source of environmental urban pollution by PGEs. This work reports on the catalyst morphology through changes in catalyst surface by scanning electron microscopy/energy dispersive X-ray spectroscopy (SEM/EDX) and laser-induced breakdown spectrometry (LIBS) from fresh to aged catalytic converters. The distribution of these elements in the fresh catalysts analysed (PtPdRh gasoline catalyst) is not uniform and occurs mainly in a longitudinal direction. This heterogeneity seems to be greater for Pt and Pd. PGEs released by the catalysts, fresh and aged 30 000 km, were studied in parallel. Whole raw exhaust fumes from four catalysts of three different types were also examined. Two of these were gasoline catalysts (PtPdRh and PdRh) and the other two were diesel catalysts (Pt). Samples were collected following the 91441 EUDC driving cycle for light-duty vehicle testing. The results show that at 0 km the samples collected first have the highest content of particulate PGEs and although the general tendency is for the release to decrease with increasing number of samples taken, exceptions are frequent. At 30 000 km the released PGEs in gasoline and diesel catalysts decreased significantly. For fresh gasoline catalysts the mean of the total amount released was approximately 100, 250 and 50 ng km−1 for Pt, Pd and Rh, respectively. In diesel catalysts the Pt release varied in the range 400800 ng km−1. After ageing the catalysts up to 30 000 km, the gasoline catalysts released amounts of Pt between 6 and 8 ng km−1, Pd between 12 and 16 ng km−1 and Rh between 3 and 12 ng km−1. In diesel catalysts the Pt release varied in the range 108150 ng km−1. The soluble portion of PGEs in the HNO3 collector solution represented less than 5% of the total amount for fresh catalysts. For 30 000 km the total amount of soluble PGEs released was similar or slightly higher than for 0 km.
  •  
18.
  • Steg, Linda, et al. (författare)
  • A method to identify barriers to and enablers of implementing climate change mitigation options
  • 2022
  • Ingår i: One Earth. - : Elsevier BV. - 2590-3330 .- 2590-3322. ; 5:11, s. 1216-1227
  • Forskningsöversikt (refereegranskat)abstract
    • Mitigation option are not yet being implemented at the scale required to limit global warming to well below 2°C. Various factors have been identified that inhibit the implementation of specific mitigation options. Yet, an integrated assessment of key barriers and enablers is lacking. Here we present a comprehensive framework to assess which factors inhibit and enable the implementation of mitigation options. The framework comprises six dimensions, each encompassing different criteria: geophysical, environmental-ecological, technological, economic, sociocultural, and institutional feasibility. We demonstrate the approach by assessing to what extent each criterion and dimension affects the feasibility of six mitigation options. The assessment reveals that institutional factors inhibit the implementation of many options that need to be addressed to increase their feasibility. Of all the options assessed, many factors enable the implementation of solar energy, while only a few barriers would need to be addressed to implement solar energy at scale.
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 1-18 av 18

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy