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4. Central core disease: clinical, pathological, and genetic features

Author

Quinlivan, R.M., Muller, C.R., Davis, M., Laing, N.G., Evans, G.A., Dwyer, J., Dove, J., Roberts, A.P., and Sewry, C.A.

Subjects
Diagnosis, Development and progression, Research, Genetic aspects, Genetic disorders -- Research -- Genetic aspects -- Diagnosis -- Development and progression, Muscular diseases -- Genetic aspects -- Diagnosis -- Development and progression -- Research, Muscle diseases -- Genetic aspects -- Diagnosis -- Development and progression -- Research
Abstract

Arch Dis Child 2003;88:1051-1055 Central core disease (CCD) is a dominantly inherited congenital myopathy allelic to malignant hyperthermia (MH) caused by mutations in the RYR1 gene on chromosome 19q13.1. Eleven [...]

Published
2003

5. EAU-ESMO consensus statements on the management of advanced and variant bladder cancer-an international collaborative multi-stakeholder effort: under the auspices of the EAU and ESMO Guidelines Committeesdagger

Author

Horwich, A., Babjuk, M., Bellmunt, J., Bruins, H.M., Reijke, T.M. de, Santis, M. de, Gillessen, S., James, N., MacLennan, S., Palou, J., Powles, T., Ribal, M.J., Shariat, S.F., Kwast, T.V., Xylinas, E., Agarwal, N., Arends, T.J., Bamias, A., Birtle, A., Black, P.C., Bochner, B.H., Bolla, M., Boormans, J.L., Bossi, A., Briganti, A., Brummelhuis, I., Burger, M., Castellano, D., Cathomas, R., Chiti, A., Choudhury, A., Comperat, E., Crabb, S., Culine, S., Bari, B. De, Blok, W., Visschere, P.J. De, Decaestecker, K., Dimitropoulos, K., Dominguez-Escrig, J.L., Fanti, S., Fonteyne, V., Frydenberg, M., Fütterer, J.J., Gakis, G., Geavlete, B., Gontero, P., Grubmuller, B., Hafeez, S., Hansel, D.E., Hartmann, A., Hayne, D., Henry, A.M., Hernandez, V., Herr, H., Herrmann, K., Hoskin, P., Huguet, J., Jereczek-Fossa, B.A., Jones, R., Kamat, A.M., Khoo, V., Kiltie, A.E., Krege, S., Ladoire, S., Lara, P.C., Leliveld, A., Linares-Espinos, E., Logager, V., Lorch, A., Loriot, Y., Meijer, R., Mir, M.C., Moschini, M., Mostafid, H, Muller, A.C., Muller, C.R., N'Dow, J., Necchi, A., Neuzillet, Y., Oddens, J.R., Oldenburg, J., Osanto, S., Oyen, W.J., Pacheco-Figueiredo, L., Pappot, H., Patel, M.I., Pieters, B.R., Plass, K., Remzi, M., Retz, M., Richenberg, J., Rink, M., Roghmann, F., Rosenberg, J.E., Roupret, M., Rouviere, O., Salembier, C., Salminen, A., Sargos, P., Smeenk, R.J., Heijden, A.G. van der, Witjes, J.A., Horwich, A., Babjuk, M., Bellmunt, J., Bruins, H.M., Reijke, T.M. de, Santis, M. de, Gillessen, S., James, N., MacLennan, S., Palou, J., Powles, T., Ribal, M.J., Shariat, S.F., Kwast, T.V., Xylinas, E., Agarwal, N., Arends, T.J., Bamias, A., Birtle, A., Black, P.C., Bochner, B.H., Bolla, M., Boormans, J.L., Bossi, A., Briganti, A., Brummelhuis, I., Burger, M., Castellano, D., Cathomas, R., Chiti, A., Choudhury, A., Comperat, E., Crabb, S., Culine, S., Bari, B. De, Blok, W., Visschere, P.J. De, Decaestecker, K., Dimitropoulos, K., Dominguez-Escrig, J.L., Fanti, S., Fonteyne, V., Frydenberg, M., Fütterer, J.J., Gakis, G., Geavlete, B., Gontero, P., Grubmuller, B., Hafeez, S., Hansel, D.E., Hartmann, A., Hayne, D., Henry, A.M., Hernandez, V., Herr, H., Herrmann, K., Hoskin, P., Huguet, J., Jereczek-Fossa, B.A., Jones, R., Kamat, A.M., Khoo, V., Kiltie, A.E., Krege, S., Ladoire, S., Lara, P.C., Leliveld, A., Linares-Espinos, E., Logager, V., Lorch, A., Loriot, Y., Meijer, R., Mir, M.C., Moschini, M., Mostafid, H, Muller, A.C., Muller, C.R., N'Dow, J., Necchi, A., Neuzillet, Y., Oddens, J.R., Oldenburg, J., Osanto, S., Oyen, W.J., Pacheco-Figueiredo, L., Pappot, H., Patel, M.I., Pieters, B.R., Plass, K., Remzi, M., Retz, M., Richenberg, J., Rink, M., Roghmann, F., Rosenberg, J.E., Roupret, M., Rouviere, O., Salembier, C., Salminen, A., Sargos, P., Smeenk, R.J., Heijden, A.G. van der, and Witjes, J.A.

Abstract

Contains fulltext : 215784.pdf (publisher's version ) (Closed access), BACKGROUND: Although guidelines exist for advanced and variant bladder cancer management, evidence is limited/conflicting in some areas and the optimal approach remains controversial. OBJECTIVE: To bring together a large multidisciplinary group of experts to develop consensus statements on controversial topics in bladder cancer management. DESIGN: A steering committee compiled proposed statements regarding advanced and variant bladder cancer management which were assessed by 113 experts in a Delphi survey. Statements not reaching consensus were reviewed; those prioritised were revised by a panel of 45 experts before voting during a consensus conference. SETTING: Online Delphi survey and consensus conference. PARTICIPANTS: The European Association of Urology (EAU), the European Society for Medical Oncology (ESMO), experts in bladder cancer management. OUTCOME MEASUREMENTS AND STATISTICAL ANALYSIS: Statements were ranked by experts according to their level of agreement: 1-3 (disagree), 4-6 (equivocal), 7-9 (agree). A priori (level 1) consensus was defined as >/=70% agreement and

Published
2019

6. Large scale multifactorial likelihood quantitative analysis of BRCA1 and BRCA2 variants: An ENIGMA resource to support clinical variant classification.

Author

Feroce I., Schoenwiese U., Seggewiss J., Solanes A., Steinemann D., Stiller M., Stoppa-Lyonnet D., Sullivan K.J., Susman R., Sutter C., Tavtigian S.V., Teo S.H., Teule A., Thomassen M., Tibiletti M.G., Tischkowitz M., Tognazzo S., Toland A.E., Tornero E., Torngren T., Torres-Esquius S., Toss A., Trainer A.H., Tucker K.M., van Asperen C.J., van Mackelenbergh M.T., Varesco L., Vargas-Parra G., Varon R., Vega A., Velasco A., Vesper A.-S., Viel A., Vreeswijk M.P.G., Wagner S.A., Waha A., Walker L.C., Walters R.J., Wang-Gohrke S., Weber B.H.F., Weichert W., Wieland K., Wiesmuller L., Witzel I., Wockel A., Woodward E.R., Zachariae S., Zampiga V., Zeder-Goss C., Investigators K., Lazaro C., De Nicolo A., Radice P., Engel C., Schmutzler R.K., Goldgar D.E., Spurdle A.B., Harris M., Parsons M.T., Tudini E., Li H., Hahnen E., Wappenschmidt B., Feliubadalo L., Aalfs C.M., Agata S., Aittomaki K., Alducci E., Alonso-Cerezo M.C., Arnold N., Auber B., Austin R., Azzollini J., Balmana J., Barbieri E., Bartram C.R., Blanco A., Blumcke B., Bonache S., Bonanni B., Borg A., Bortesi B., Brunet J., Bruzzone C., Bucksch K., Cagnoli G., Caldes T., Caliebe A., Caligo M.A., Calvello M., Capone G.L., Caputo S.M., Carnevali I., Carrasco E., Caux-Moncoutier V., Cavalli P., Cini G., Clarke E.M., Concolino P., Cops E.J., Cortesi L., Couch F.J., Darder E., de la Hoya M., Dean M., Debatin I., Del Valle J., Delnatte C., Derive N., Diez O., Ditsch N., Domchek S.M., Dutrannoy V., Eccles D.M., Ehrencrona H., Enders U., Evans D.G., Farra C., Faust U., Felbor U., Fine M., Foulkes W.D., Galvao H.C.R., Gambino G., Gehrig A., Gensini F., Gerdes A.-M., Germani A., Giesecke J., Gismondi V., Gomez C., Gomez Garcia E.B., Gonzalez S., Grau E., Grill S., Gross E., Guerrieri-Gonzaga A., Guillaud-Bataille M., Gutierrez-Enriquez S., Haaf T., Hackmann K., Hansen T.V.O., Hauke J., Heinrich T., Hellebrand H., Herold K.N., Honisch E., Horvath J., Houdayer C., Hubbel V., Iglesias S., Izquierdo A., James P.A., Janssen L.A.M., Jeschke U., Kaulfuss S., Keupp K., Kiechle M., Kolbl A., Krieger S., Kruse T.A., Kvist A., Lalloo F., Larsen M., Lattimore V.L., Lautrup C., Ledig S., Leinert E., Lewis A.L., Lim J., Loeffler M., Lopez-Fernandez A., Lucci-Cordisco E., Maass N., Manoukian S., Marabelli M., Matricardi L., Meindl A., Michelli R.D., Moghadasi S., Moles-Fernandez A., Montagna M., Montalban G., Monteiro A.N., Montes E., Mori L., Moserle L., Muller C.R., Mundhenke C., Naldi N., Nathanson K.L., Navarro M., Nevanlinna H., Nichols C.B., Niederacher D., Nielsen H.R., Ong K.-R., Pachter N., Palmero E.I., Papi L., Pedersen I.S., Peissel B., Perez-Segura P., Pfeifer K., Pineda M., Pohl-Rescigno E., Poplawski N.K., Porfirio B., Quante A.S., Ramser J., Reis R.M., Revillion F., Rhiem K., Riboli B., Ritter J., Rivera D., Rofes P., Rump A., Salinas M., Sanchez de Abajo A.M., Schmidt G., Feroce I., Schoenwiese U., Seggewiss J., Solanes A., Steinemann D., Stiller M., Stoppa-Lyonnet D., Sullivan K.J., Susman R., Sutter C., Tavtigian S.V., Teo S.H., Teule A., Thomassen M., Tibiletti M.G., Tischkowitz M., Tognazzo S., Toland A.E., Tornero E., Torngren T., Torres-Esquius S., Toss A., Trainer A.H., Tucker K.M., van Asperen C.J., van Mackelenbergh M.T., Varesco L., Vargas-Parra G., Varon R., Vega A., Velasco A., Vesper A.-S., Viel A., Vreeswijk M.P.G., Wagner S.A., Waha A., Walker L.C., Walters R.J., Wang-Gohrke S., Weber B.H.F., Weichert W., Wieland K., Wiesmuller L., Witzel I., Wockel A., Woodward E.R., Zachariae S., Zampiga V., Zeder-Goss C., Investigators K., Lazaro C., De Nicolo A., Radice P., Engel C., Schmutzler R.K., Goldgar D.E., Spurdle A.B., Harris M., Parsons M.T., Tudini E., Li H., Hahnen E., Wappenschmidt B., Feliubadalo L., Aalfs C.M., Agata S., Aittomaki K., Alducci E., Alonso-Cerezo M.C., Arnold N., Auber B., Austin R., Azzollini J., Balmana J., Barbieri E., Bartram C.R., Blanco A., Blumcke B., Bonache S., Bonanni B., Borg A., Bortesi B., Brunet J., Bruzzone C., Bucksch K., Cagnoli G., Caldes T., Caliebe A., Caligo M.A., Calvello M., Capone G.L., Caputo S.M., Carnevali I., Carrasco E., Caux-Moncoutier V., Cavalli P., Cini G., Clarke E.M., Concolino P., Cops E.J., Cortesi L., Couch F.J., Darder E., de la Hoya M., Dean M., Debatin I., Del Valle J., Delnatte C., Derive N., Diez O., Ditsch N., Domchek S.M., Dutrannoy V., Eccles D.M., Ehrencrona H., Enders U., Evans D.G., Farra C., Faust U., Felbor U., Fine M., Foulkes W.D., Galvao H.C.R., Gambino G., Gehrig A., Gensini F., Gerdes A.-M., Germani A., Giesecke J., Gismondi V., Gomez C., Gomez Garcia E.B., Gonzalez S., Grau E., Grill S., Gross E., Guerrieri-Gonzaga A., Guillaud-Bataille M., Gutierrez-Enriquez S., Haaf T., Hackmann K., Hansen T.V.O., Hauke J., Heinrich T., Hellebrand H., Herold K.N., Honisch E., Horvath J., Houdayer C., Hubbel V., Iglesias S., Izquierdo A., James P.A., Janssen L.A.M., Jeschke U., Kaulfuss S., Keupp K., Kiechle M., Kolbl A., Krieger S., Kruse T.A., Kvist A., Lalloo F., Larsen M., Lattimore V.L., Lautrup C., Ledig S., Leinert E., Lewis A.L., Lim J., Loeffler M., Lopez-Fernandez A., Lucci-Cordisco E., Maass N., Manoukian S., Marabelli M., Matricardi L., Meindl A., Michelli R.D., Moghadasi S., Moles-Fernandez A., Montagna M., Montalban G., Monteiro A.N., Montes E., Mori L., Moserle L., Muller C.R., Mundhenke C., Naldi N., Nathanson K.L., Navarro M., Nevanlinna H., Nichols C.B., Niederacher D., Nielsen H.R., Ong K.-R., Pachter N., Palmero E.I., Papi L., Pedersen I.S., Peissel B., Perez-Segura P., Pfeifer K., Pineda M., Pohl-Rescigno E., Poplawski N.K., Porfirio B., Quante A.S., Ramser J., Reis R.M., Revillion F., Rhiem K., Riboli B., Ritter J., Rivera D., Rofes P., Rump A., Salinas M., Sanchez de Abajo A.M., and Schmidt G.

Abstract

The multifactorial likelihood analysis method has demonstrated utility for quantitative assessment of variant pathogenicity for multiple cancer syndrome genes. Independent data types currently incorporated in the model for assessing BRCA1 and BRCA2 variants include clinically calibrated prior probability of pathogenicity based on variant location and bioinformatic prediction of variant effect, co-segregation, family cancer history profile, co-occurrence with a pathogenic variant in the same gene, breast tumor pathology, and case-control information. Research and clinical data for multifactorial likelihood analysis were collated for 1,395 BRCA1/2 predominantly intronic and missense variants, enabling classification based on posterior probability of pathogenicity for 734 variants: 447 variants were classified as (likely) benign, and 94 as (likely) pathogenic; and 248 classifications were new or considerably altered relative to ClinVar submissions. Classifications were compared with information not yet included in the likelihood model, and evidence strengths aligned to those recommended for ACMG/AMP classification codes. Altered mRNA splicing or function relative to known nonpathogenic variant controls were moderately to strongly predictive of variant pathogenicity. Variant absence in population datasets provided supporting evidence for variant pathogenicity. These findings have direct relevance for BRCA1 and BRCA2 variant evaluation, and justify the need for gene-specific calibration of evidence types used for variant classification.Copyright © 2019 Wiley Periodicals, Inc.

Published
2019

7. Early and lethal neurodegeneration with myasthenic and myopathic features: A new ALG14-CDG

Author

Schorling, D.C., Rost, S., Lefeber, D.J., Brady, L., Muller, C.R., Korinthenberg, R., Tarnopolsky, M., Bonnemann, C.G., Rodenburg, R.J.T., Bugiani, M., Beytia, M., Kruger, M., Knaap, M. van der, Kirschner, J., Schorling, D.C., Rost, S., Lefeber, D.J., Brady, L., Muller, C.R., Korinthenberg, R., Tarnopolsky, M., Bonnemann, C.G., Rodenburg, R.J.T., Bugiani, M., Beytia, M., Kruger, M., Knaap, M. van der, and Kirschner, J.

Abstract

Item does not contain fulltext, OBJECTIVE: To describe the presentation and identify the cause of a new clinical phenotype, characterized by early severe neurodegeneration with myopathic and myasthenic features. METHODS: This case study of 5 patients from 3 families includes clinical phenotype, serial MRI, electrophysiologic testing, muscle biopsy, and full autopsy. Genetic workup included whole exome sequencing and segregation analysis of the likely causal mutation. RESULTS: All 5 patients showed severe muscular hypotonia, progressive cerebral atrophy, and therapy-refractory epilepsy. Three patients had congenital contractures. All patients died during their first year of life. In 2 of our patients, electrophysiologic testing showed abnormal decrement, but treatment with pyridostigmine led only to temporary improvement. Causative mutations in ALG14 were identified in all patients. The mutation c.220 G>A (p.Asp74Asn) was homozygous in 2 patients and heterozygous in the other 3 patients. Additional heterozygous mutations were c.422T>G (p.Val141Gly) and c.326G>A (p.Arg109Gln). In all cases, parents were found to be heterozygous carriers. None of the identified variants has been described previously. CONCLUSIONS: We report a genetic syndrome combining myasthenic features and severe neurodegeneration with therapy-refractory epilepsy. The underlying cause is a glycosylation defect due to mutations in ALG14. These cases broaden the phenotypic spectrum associated with ALG14 congenital disorders of glycosylation as previously only isolated myasthenia has been described.

Published
2017

8. Analysis of mRNA in hemophilia A patients with undetectable mutations reveals normal splicing in the factor VIII gene

Author

El-Maarri, O., Herbiniaux, U., Graw, J., Schroder, J., Terzic, A., Watzka, M., Brackmann, H.H., Schramm, W., Hanfland, P., Schwaab, R., Muller, C.R., Oldenburg, J., El-Maarri, O., Herbiniaux, U., Graw, J., Schroder, J., Terzic, A., Watzka, M., Brackmann, H.H., Schramm, W., Hanfland, P., Schwaab, R., Muller, C.R., and Oldenburg, J.

Abstract

Background: haemophilia A (HA) is characterized by partial or total deficiency of factor VIII (FVIII) protein activity. It is caused by a broad spectrum of mutations in the FVIII gene. Despite tremendous improvements in mutation screening methods, in about 2% of HA patients no DNA change could be found, even after sequencing the whole coding part of the FVIII gene including the flanking splice sites, as well as the promotor and the 3′ UTR regions. Objectives, patients and methods: In the present study we performed a detailed RNA analysis of three groups of patients. The first included control patients with known splicing defects, the second included two patients with already identified nucleotide changes close to splicing sites, that could potentially alter the normal splicing process, and a third group of 11 unrelated patients whose genomic DNA have already been screened for mutations by DHPLC and direct sequencing with no mutation being identified. Results: Both candidate splice site mutations were shown to result in either skipping or alternative splicing of at least one exon, therefore these DNA changes must be considered as causal for the patients' HA phenotype. In contrast, no abnormalities on the RNA level were observed in any of 11 unrelated patients without mutations in the FVIII gene. Conclusions: These findings exclude mutations that could be located deep in the introns and affecting either normal splicing or lead to mechanisms causing some unknown rearrangements of the FVIII gene. In fact, our results point to the presence of still unknown factor(s) causing HA, which might be either allelic or in the close proximity of the FVIII gene or non-allelic associated with other genetic loci that are involved in the processing of the FVIII protein.

Published
2017

9. Factor VIII intron-1 inversion

Author

El Maarri, O., Schroder, J., Schwaab, R., Muller, C.R., Oldenburg, J., El Maarri, O., Schroder, J., Schwaab, R., Muller, C.R., and Oldenburg, J.

Published
2017

10. A standardized framework for the validation and verification of clinical molecular genetic tests.

Author

Mattocks, C.J., Morris, M.A., Matthijs, G., Swinnen, E., Corveleyn, A., Dequeker, E., Muller, C.R., Pratt, V., Wallace, A., Mattocks, C.J., Morris, M.A., Matthijs, G., Swinnen, E., Corveleyn, A., Dequeker, E., Muller, C.R., Pratt, V., and Wallace, A.

Abstract

01 december 2010, Item does not contain fulltext, The validation and verification of laboratory methods and procedures before their use in clinical testing is essential for providing a safe and useful service to clinicians and patients. This paper outlines the principles of validation and verification in the context of clinical human molecular genetic testing. We describe implementation processes, types of tests and their key validation components, and suggest some relevant statistical approaches that can be used by individual laboratories to ensure that tests are conducted to defined standards.

Published
2010

11. Recognizing and managing a malignant hyperthermia crisis: guidelines from the European Malignant Hyperthermia Group

Author

Glahn, K P E, Ellis, F.R., Halsall, P.J., Muller, C.R., Snoeck, M.M.J., Urwyler, A., Wappler, F., Glahn, K P E, Ellis, F.R., Halsall, P.J., Muller, C.R., Snoeck, M.M.J., Urwyler, A., and Wappler, F.

Abstract

Survival from a malignant hyperthermia (MH) crisis is highly dependent on early recognition and prompt action. MH crises are very rare and an increasing use of total i.v. anaesthesia is likely to make it even rarer, leading to the potential risk of reduced awareness of MH. In addition, dantrolene, the cornerstone of successful MH treatment, is unavailable in large areas around the world thereby increasing the risk of MH fatalities in these areas. The European Malignant Hyperthermia Group collected and reviewed all guidelines available from the various MH centres in order to provide a consensus document. The guidelines consist of two textboxes: Box 1 on recognizing MH and Box 2 on the treatment of an MH crisis

Published
2010

16. A genetic linkage map of five marker loci in and around the Duchenne muscular dystrophy locus

Author

Chen, J.D., primary, Hejtmancik, J.F., additional, Romeo, G., additional, Lindlof, M., additional, Boehm, C., additional, Caskey, C.T., additional, Kress, W., additional, Fischbeck, K.H., additional, Dreier, M., additional, Serravalle, S., additional, Grimm, T., additional, Kaariainen, H., additional, Ferrari, M., additional, Pfendner, E., additional, Meng, G., additional, de la Chapelle, A., additional, Melis, M.A., additional, Muller, B., additional, MacKinlay, A.G., additional, Muller, C.R., additional, and Denton, M.J., additional

Published
1989
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18. Effect of molten sodium nitrate on the decomposition pathways of hydrated magnesium hydroxycarbonate to magnesium oxide probed by in situ total scattering

Author

Paula M. Abdala, Zhu-Jun Wang, Alessandro Dal Pozzo, Andac Armutlulu, Margarita Rekhtina, Alexey Fedorov, Felix Donat, Marc Georg Willinger, Christoph R. Müller, Maria Valeria Blanco, Dragos Stoian, Rekhtina M., Dal Pozzo A., Stoian D., Armutlulu A., Donat F., Blanco M.V., Wang Z.-J., Willinger M.-G., Fedorov A., Abdala P.M., and Muller C.R.

Subjects
Magnesium oxide Decomposition In situ total scattering CO2 capture, Thermogravimetric analysis, Materials science, Magnesium, Thermal decomposition, chemistry.chemical_element, 02 engineering and technology, 010402 general chemistry, 021001 nanoscience & nanotechnology, 01 natural sciences, Decomposition, 3. Good health, 0104 chemical sciences, law.invention, Chemical engineering, chemistry, law, Water of crystallization, General Materials Science, Crystallite, Hydromagnesite, Crystallization, 0210 nano-technology
Abstract

The effect of NaNO3 and its physical state on the thermal decomposition pathways of hydrated magnesium hydroxycarbonate (hydromagnesite, HM) towards MgO was examined by in situ total scattering. Pair distribution function (PDF) analysis of these data allowed us to probe the structural evolution of pristine and NaNO3-promoted HM. A multivariate curve resolution alternating least squares (MCR-ALS) analysis identified the intermediate phases and their evolution upon the decomposition of both precursors to MgO. The total scattering results are discussed in relation with thermogravimetric measurements coupled with off-gas analysis. MgO is obtained from pristine HM (N2, 10 °C min−1) through an amorphous magnesium carbonate intermediate (AMC), formed after the partial removal of water of crystallization from HM. The decomposition continues via a gradual release of water (due to dehydration and dehydroxylation) and, in the last step, via decarbonation, leading to crystalline MgO. The presence of molten NaNO3 alters the decomposition pathways of HM, proceeding now through AMC and crystalline MgCO3. These results demonstrate that molten NaNO3 facilitates the release of water (from both water of crystallization and through dehydroxylation) and decarbonation, and promotes the crystallization of MgCO3 and MgO in comparison to pristine HM. MgO formed from the pristine HM precursor shows a smaller average crystallite size than NaNO3-promoted HM and preserves the initial nano-plate-like morphology of HM. NaNO3-promoted HM was decomposed to MgO that is characterized by a larger average crystallite size and irregular morphology. Additionally, in situ SEM allowed visualization of the morphological evolution of HM promoted with NaNO3 at a micrometre scale., Nanoscale, 12 (31), ISSN:2040-3364, ISSN:2040-3372

Published
2020

19. CO2 Uptake and Cyclic Stability of MgO-Based CO2 Sorbents Promoted with Alkali Metal Nitrates and Their Eutectic Mixtures

Author

Paula M. Abdala, Margarita Rekhtina, Andac Armutlulu, Christoph R. Müller, Alessandro Dal Pozzo, Dal Pozzo A., Armutlulu A., Rekhtina M., Abdala P.M., and Muller C.R.

Subjects
Materials science, MgO, Energy Engineering and Power Technology, Context (language use), 02 engineering and technology, 010402 general chemistry, 01 natural sciences, Materials Chemistry, Electrochemistry, Chemical Engineering (miscellaneous), Electrical and Electronic Engineering, Cyclic stability, Eutectic system, molten salts, 021001 nanoscience & nanotechnology, Alkali metal, CO2 capture, 3. Good health, 0104 chemical sciences, Chemical engineering, alkali metal nitrate, cyclic stability, deactivation, Greenhouse gas, 0210 nano-technology
Abstract

ACS Applied Energy Materials, 2 (2), ISSN:2574-0962

Published
2019

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