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  1. Article ; Online: Nanoplastics released from daily used silicone and latex products during mechanical breakdown.

    Ekvall, Mikael T / Gimskog, Isabella / Kelpsiene, Egle / Mellring, Alice / Månsson, Alma / Lundqvist, Martin / Cedervall, Tommy

    PloS one

    2023  Volume 18, Issue 9, Page(s) e0289377

    Abstract: Waste of polymer products, especially plastics, in nature has become a problem that caught the awareness of the general public during the last decade. The macro- and micro polymers in nature will be broken down by naturally occurring events such as ... ...

    Abstract Waste of polymer products, especially plastics, in nature has become a problem that caught the awareness of the general public during the last decade. The macro- and micro polymers in nature will be broken down by naturally occurring events such as mechanical wear and ultra-violet (UV) radiation which will result in the generation of polymeric particles in the nano-size range. We have recently shown that polystyrene and high-density polyethylene macroplastic can be broken down into nano-sized particles by applying mechanical force from an immersion blender. In this article, we show that particles in the nano-size range are released from silicone and latex pacifiers after the same treatment. Additionally, boiling the pacifiers prior to the mechanical breakdown process results in an increased number of particles released from the silicone but not the latex pacifier. Particles from the latex pacifier are acutely toxic to the freshwater filter feeding zooplankter Daphnia magna.
    MeSH term(s) Animals ; Latex ; Microplastics/toxicity ; Polymers ; Daphnia ; Silicones
    Chemical Substances Latex ; Microplastics ; Polymers ; Silicones
    Language English
    Publishing date 2023-09-13
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2267670-3
    ISSN 1932-6203 ; 1932-6203
    ISSN (online) 1932-6203
    ISSN 1932-6203
    DOI 10.1371/journal.pone.0289377
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Skin mesenchymal niches maintain and protect AML-initiating stem cells.

    Sandhow, Lakshmi / Cai, Huan / Leonard, Elory / Xiao, Pingnan / Tomaipitinca, Luana / Månsson, Alma / Kondo, Makoto / Sun, Xiaoyan / Johansson, Anne-Sofie / Tryggvason, Karl / Kasper, Maria / Järås, Marcus / Qian, Hong

    The Journal of experimental medicine

    2023  Volume 220, Issue 10

    Abstract: Leukemia cutis or leukemic cell infiltration in skin is one of the common extramedullary manifestations of acute myeloid leukemia (AML) and signifies a poorer prognosis. However, its pathogenesis and maintenance remain understudied. Here, we report ... ...

    Abstract Leukemia cutis or leukemic cell infiltration in skin is one of the common extramedullary manifestations of acute myeloid leukemia (AML) and signifies a poorer prognosis. However, its pathogenesis and maintenance remain understudied. Here, we report massive AML cell infiltration in the skin in a transplantation-induced MLL-AF9 AML mouse model. These AML cells could regenerate AML after transplantation. Prospective niche characterization revealed that skin harbored mesenchymal progenitor cells (MPCs) with a similar phenotype as BM mesenchymal stem cells. These skin MPCs protected AML-initiating stem cells (LSCs) from chemotherapy in vitro partially via mitochondrial transfer. Furthermore, Lama4 deletion in skin MPCs promoted AML LSC proliferation and chemoresistance. Importantly, more chemoresistant AML LSCs appeared to be retained in Lama4-/- mouse skin after cytarabine treatment. Our study reveals the characteristics and previously unrecognized roles of skin mesenchymal niches in maintaining and protecting AML LSCs during chemotherapy, meriting future exploration of their impact on AML relapse.
    MeSH term(s) Animals ; Mice ; Prospective Studies ; Stem Cells ; Skin ; Leukemia, Myeloid, Acute ; Mesenchymal Stem Cells
    Language English
    Publishing date 2023-07-26
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218343-2
    ISSN 1540-9538 ; 0022-1007
    ISSN (online) 1540-9538
    ISSN 0022-1007
    DOI 10.1084/jem.20220953
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Characterization of the bone marrow niche in patients with chronic myeloid leukemia identifies CXCL14 as a new therapeutic option.

    Dolinska, Monika / Cai, Huan / Månsson, Alma / Shen, Jingyi / Xiao, Pingnan / Bouderlique, Thibault / Li, Xidan / Leonard, Elory / Chang, Marcus / Gao, Yuchen / Medina, Juan Pablo / Kondo, Makoto / Sandhow, Lakshmi / Johansson, Anne-Sofie / Deneberg, Stefan / Söderlund, Stina / Jädersten, Martin / Ungerstedt, Johanna / Tobiasson, Magnus /
    Östman, Arne / Mustjoki, Satu / Stenke, Leif / Le Blanc, Katarina / Hellström-Lindberg, Eva / Lehmann, Sören / Ekblom, Marja / Olsson-Strömberg, Ulla / Sigvardsson, Mikael / Qian, Hong

    Blood

    2023  Volume 142, Issue 1, Page(s) 73–89

    Abstract: Although tyrosine kinase inhibitors (TKIs) are effective in treating chronic myeloid leukemia (CML), they often fail to eradicate the leukemia-initiating stem cells (LSCs), causing disease persistence and relapse. Evidence indicates that LSC persistence ... ...

    Abstract Although tyrosine kinase inhibitors (TKIs) are effective in treating chronic myeloid leukemia (CML), they often fail to eradicate the leukemia-initiating stem cells (LSCs), causing disease persistence and relapse. Evidence indicates that LSC persistence may be because of bone marrow (BM) niche protection; however, little is known about the underlying mechanisms. Herein, we molecularly and functionally characterize BM niches in patients with CML at diagnosis and reveal the altered niche composition and function in these patients. Long-term culture initiating cell assay showed that the mesenchymal stem cells from patients with CML displayed an enhanced supporting capacity for normal and CML BM CD34+CD38- cells. Molecularly, RNA sequencing detected dysregulated cytokine and growth factor expression in the BM cellular niches of patients with CML. Among them, CXCL14 was lost in the BM cellular niches in contrast to its expression in healthy BM. Restoring CXCL14 significantly inhibited CML LSC maintenance and enhanced their response to imatinib in vitro, and CML engraftment in vivo in NSG-SGM3 mice. Importantly, CXCL14 treatment dramatically inhibited CML engraftment in patient-derived xenografted NSG-SGM3 mice, even to a greater degree than imatinib, and this inhibition persisted in patients with suboptimal TKI response. Mechanistically, CXCL14 upregulated inflammatory cytokine signaling but downregulated mTOR signaling and oxidative phosphorylation in CML LSCs. Together, we have discovered a suppressive role of CXCL14 in CML LSC growth. CXCL14 might offer a treatment option targeting CML LSCs.
    MeSH term(s) Animals ; Mice ; Bone Marrow/metabolism ; Chemokines, CXC/metabolism ; Chemokines, CXC/pharmacology ; Chemokines, CXC/therapeutic use ; Cytokines/metabolism ; Imatinib Mesylate/pharmacology ; Imatinib Mesylate/therapeutic use ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/metabolism ; Neoplastic Stem Cells/metabolism ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Signal Transduction
    Chemical Substances Chemokines, CXC ; CXCL14 protein, mouse ; Cytokines ; Imatinib Mesylate (8A1O1M485B) ; Protein Kinase Inhibitors ; CXCL14 protein, human
    Language English
    Publishing date 2023-01-19
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2022016896
    Database MEDical Literature Analysis and Retrieval System OnLINE

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