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Nicole L. Rosin

Researcher at University of Calgary

Publications -  34
Citations -  1235

Nicole L. Rosin is an academic researcher from University of Calgary. The author has contributed to research in topics: Wound healing & Medicine. The author has an hindex of 15, co-authored 24 publications receiving 810 citations. Previous affiliations of Nicole L. Rosin include University of British Columbia & Dalhousie University.

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Macrophages and Associated Ligands in the Aged Injured Nerve: A Defective Dynamic That Contributes to Reduced Axonal Regrowth.

TL;DR: Interestingly, impairment in both macrophage accumulation and functional recovery could be overcome by transplanting bone marrow from aged animals into young mice, and the data suggest that age-associated defects in MCP1 signaling could contribute to the regenerative deficits that occur in the aged nervous system.
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Adult Human Dermal Progenitor Cell Transplantation Modulates the Functional Outcome of Split-Thickness Skin Xenografts

TL;DR: C cultured DPCs were transplanted into a full-thickness skin wound in immune-compromised mice and closed with a human STSG, improving both viscoelastic properties of the graft and mitigating pruritus.
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A B1a–natural IgG–neutrophil axis is impaired in viral- and steroid-associated aspergillosis

TL;DR: Sarden et al. as discussed by the authors investigated three distinct conditions predisposing to lethal aspergillosis, including severe SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) infection, influenza A viral pneumonia, and systemic corticosteroid use.
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Comparison of human skin‐ and nerve‐derived Schwann cells reveals many similarities and subtle genomic and functional differences

TL;DR: Skin‐derived SCs share near‐identical properties to N‐SCs but with subtle differences that could potentially enhance their therapeutic utility, and single‐cell RNA‐sequencing revealed an overwhelming overlap in gene expression with the exception of HLA genes which were preferentially up‐regulated in Sk‐ SCs.
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Antibody therapy can enhance AngiotensinII-induced myocardial fibrosis.

TL;DR: These data suggest that myocardial fibrosis was increased by the addition of exogenous non-specific antibodies in an Fc-mediated manner, which could have substantial impact on the future experimental design of antibody-based therapeutics.