| 1. |
- Baghaei, Behnaz, 1986-, et al.
(author)
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All-Cellulose Composites Properties from Pre- and Post-Consumer Denim Wastes: Comparative Study
- 2022
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In: Journal of Composites Science. - : MDPI AG. - 2504-477X. ; 6:5
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Journal article (pop. science, debate, etc.)abstract
- This study reports the recycling of discarded denim textiles by the production of all-cellulose composites (ACCs). Discarded denim fabrics were shredded into fibers and then made into nonwoven fabrics by carding and needle punching. The produced nonwoven fabrics were converted to ACCs by one-step and two-step methods using an ionic liquid (IL), 1-butyl-3-methyl imidazolium acetate ([BMIM][Ac]). In this study, the effect of different ACC manufacturing methods, denim fabrics with different contents (a 100% cotton denim (CO) and a blend material (cotton, poly-ester and elastane (BCO)) and reusing of IL as a recycled cellulose solvent on the mechanical pro-perties of the formed ACCs were investigated. The ACCs were characterized according to their tensile and impact properties, as well as their void content. Microscopic analysis was carried out to study the morphology of a cross-section of the formed composites. The choice of the one-step method with recycled IL, pure IL or with a blend material (BCO) had no influence on the tensile properties. Instead, the result showed that the two-step method, with and without DMSO, will influence the E-modulus but not the tensile strength. Regarding the impact properties of the samples, the only factor likely to influence the impact energy was the one-step method with CO and BCO.
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| 2. |
- Kehoe, Laura, et al.
(author)
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Make EU trade with Brazil sustainable
- 2019
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In: Science. - : American Association for the Advancement of Science (AAAS). - 0036-8075 .- 1095-9203. ; 364:6438, s. 341-
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Journal article (other academic/artistic)
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| 4. |
- Packer, Leisl, et al.
(author)
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Osteopontin is a downstream effector of the PI3-kinase pathway in melanomas that is inversely correlated with functional PTEN
- 2006
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In: Carcinogenesis. - : Oxford University Press (OUP). - 0143-3334 .- 1460-2180. ; 27:9, s. 1778-1786
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Journal article (peer-reviewed)abstract
- The tumor suppressor PTEN antagonizes phosphatidylinositol 3-kinase (PI3K), which contributes to tumorigenesis in many cancer types. While PTEN mutations occur in some melanomas, their precise mechanistic consequences have yet to be elucidated. We sought to identify novel downstream effectors of PI3K using a combination of genomic and functional tests. Microarray analysis of 53 melanoma cell lines identified 610 genes differentially expressed (P < 0.05) between wild-type lines and those with PTEN aberrations. Many of these genes are known to be involved in the PI3K pathway and other signaling pathways influenced by PTEN. Validation of differential gene expression by qRT-PCR was performed in the original 53 cell lines and an independent set of 18 melanoma lines with known PTEN status. Osteopontin (OPN), a secreted glycophosphoprotein that contributes to tumor progression, was more abundant at both the mRNA and protein level in PTEN mutants. The inverse correlation between OPN and PTEN expression was validated (P < 0.02) by immunohistochemistry using melanoma tissue microarrays. Finally, treatment of cell lines with the PI3K inhibitor LY294002 caused a reduction in expression of OPN. These data indicate that OPN acts downstream of PI3K in melanoma and provides insight into how PTEN loss contributes to melanoma development.
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| 5. |
- Sagar, Rachel L, et al.
(author)
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An exploratory open-label multicentre phase I/II trial evaluating the safety and efficacy of postnatal or prenatal and postnatal administration of allogeneic expanded fetal mesenchymal stem cells for the treatment of severe osteogenesis imperfecta in infants and fetuses: the BOOSTB4 trial protocol
- 2024
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In: BMJ Open. - 2044-6055. ; 14:6
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Journal article (peer-reviewed)abstract
- Introduction Severe osteogenesis imperfecta (OI) is a debilitating disease with no cure or sufficiently effective treatment. Mesenchymal stem cells (MSCs) have good safety profile, show promising effects and can form bone. The Boost Brittle Bones Before Birth (BOOSTB4) trial evaluates administration of allogeneic expanded human first trimester fetal liver MSCs (BOOST cells) for OI type 3 or severe type 4.Methods and analysis BOOSTB4 is an exploratory, open-label, multiple dose, phase I/II clinical trial evaluating safety and efficacy of postnatal (n=15) or prenatal and postnatal (n=3, originally n=15) administration of BOOST cells for the treatment of severe OI compared with a combination of historical (1–5/subject) and untreated prospective controls (≤30). Infants<18 months of age (originally<12 months) and singleton pregnant women whose fetus has severe OI with confirmed glycine substitution in COL1A1 or COL1A2 can be included in the trial.Each subject receives four intravenous doses of 3×106/kg BOOST cells at 4 month intervals, with 48 (doses 1–2) or 24 (doses 3–4) hours in-patient follow-up, primary follow-up at 6 and 12 months after the last dose and long-term follow-up yearly until 10 years after the first dose. Prenatal subjects receive the first dose via ultrasound-guided injection into the umbilical vein within the fetal liver (16+0 to 35+6 weeks), and three doses postnatally.The primary outcome measures are safety and tolerability of repeated BOOST cell administration. The secondary outcome measures are number of fractures from baseline to primary and long-term follow-up, growth, change in bone mineral density, clinical OI status and biochemical bone turnover.Ethics and dissemination The trial is approved by Competent Authorities in Sweden, the UK and the Netherlands (postnatal only). Results from the trial will be disseminated via CTIS, ClinicalTrials.gov and in scientific open-access scientific journals.Trial registration numbers EudraCT 2015-003699-60, EUCT: 2023-504593-38-00, NCT03706482.
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