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Träfflista för sökning "WFRF:(Collazo H.) "

Search: WFRF:(Collazo H.)

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1.
  • Marklund, Stellan, 1949-, et al. (author)
  • Determination of PCDDs and PCDFs in incineration samples and pyrolytic products
  • 2018
  • In: Chlorinated dioxins and dibenzofurans in perspective. - Boca Raton : CRC Press. - 9781351070645 - 9781315891545 ; , s. 79-92
  • Book chapter (peer-reviewed)abstract
    • The formation of polychlorinated dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) in municipal solid waste (MSW) incinerators is now well documented and not controversial. It is interesting to compare the PCDD and the PCDF emissions from MSW incinerators with other energy sources. The identification of lower chlorinated PCDFs like penta-CDFs in pyrolysis of hexachloroethane indicates dechlorination to be an important pathway for the formation of PCDDs and PCDFs. The environmental and human health impact of the emissions of PCDDs and PCDFs from MSW incinerators have been discussed in Umea as well as at other places in Sweden and in other countries. The laboratory pyrolysis of PVC and Saran clearly shows that PVC and other organochlorine polymers can be precursors to the PCDDs and PCDFs found in various incinerators. The chapter discusses some of the data collected so far for various types of incinerators or incineration models.
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2.
  • Prudencio, Mercedes, et al. (author)
  • Toward allele-specific targeting therapy and pharmacodynamic marker for spinocerebellar ataxia type 3
  • 2020
  • In: Science Translational Medicine. - : American Association for the Advancement of Science (AAAS). - 1946-6242 .- 1946-6234. ; 12:566
  • Journal article (peer-reviewed)abstract
    • Spinocerebellar ataxia type 3 (SCA3), caused by a CAG repeat expansion in the ataxin-3 gene (ATXN3), is characterized by neuronal polyglutamine (polyQ) ATXN3 protein aggregates. Although there is no cure for SCA3, gene-silencing approaches to reduce toxic polyQ ATXN3 showed promise in preclinical models. However, a major limitation in translating putative treatments for this rare disease to the clinic is the lack of pharmacodynamic markers for use in clinical trials. Here, we developed an immunoassay that readily detects polyQ ATXN3 proteins in human biological fluids and discriminates patients with SCA3 from healthy controls and individuals with other ataxias. We show that polyQ ATXN3 serves as a marker of target engagement in human fibroblasts, which may bode well for its use in clinical trials. Last, we identified a single-nucleotide polymorphism that strongly associates with the expanded allele, thus providing an exciting drug target to abrogate detrimental events initiated by mutant ATXN3. Gene-silencing strategies for several repeat diseases are well under way, and our results are expected to improve clinical trial preparedness for SCA3 therapies.
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