sj-docx-3-spo-10.1177_17479541231213540 - Supplemental material for A coach's perspective on augmented feedback (and technology) in cricket

Supplemental material, sj-docx-3-spo-10.1177_17479541231213540 for A coach's perspective on augmented feedback (and technology) in cricket by Kevin Tissera, Dominic Orth, Minh Huynh and Amanda C Benson in International Journal of Sports Science & Coaching</p

sj-docx-2-spo-10.1177_17479541231213540 - Supplemental material for A coach's perspective on augmented feedback (and technology) in cricket

Supplemental material, sj-docx-2-spo-10.1177_17479541231213540 for A coach's perspective on augmented feedback (and technology) in cricket by Kevin Tissera, Dominic Orth, Minh Huynh and Amanda C Benson in International Journal of Sports Science & Coaching</p

sj-docx-1-spo-10.1177_17479541231213540 - Supplemental material for A coach's perspective on augmented feedback (and technology) in cricket

Supplemental material, sj-docx-1-spo-10.1177_17479541231213540 for A coach's perspective on augmented feedback (and technology) in cricket by Kevin Tissera, Dominic Orth, Minh Huynh and Amanda C Benson in International Journal of Sports Science & Coaching</p

sj-docx-1-psg-10.1177_22925503231201631 - Supplemental material for Immediate Versus Delayed Mobilization After Cubital Tunnel Release Surgery: A Systematic Review and Meta-analysis

Supplemental material, sj-docx-1-psg-10.1177_22925503231201631 for Immediate Versus Delayed Mobilization After Cubital Tunnel Release Surgery: A Systematic Review and Meta-analysis by Oluwatobi R. Olaiya, Minh Huynh, Tega Ebeye, Lucas Gallo, Lawrence Mbuagbaw and Matthew McRae in Plastic Surgery</p

AraC induces differentiation predominantly in primary AML blasts with oncogenic <i>NRAS</i>.

<p>(A) Left panel: Example of gating for lymphocytes (LC) and AML blasts (BL) according to SSC/CD45 signals after live gating. wt<i>RAS</i> panels: CD11c expression of wt<i>RAS</i> AML blasts (left) and LC (right) in untreated samples (solid grey curve) or samples treated with 100 nM AraC (black line). mt<i>RAS</i> panels: CD11c expression of mt<i>NRAS</i>12/13 blasts (left) and LC (right) treated as indicated above. (B) Summary of the <i>in vitro</i> responses to AraC treatment in terms of differentiation of 22 primary AML blasts with or without <i>NRAS</i> mutation. <i>Samples with differentiation</i> describes the portion of samples with differentiation response (diff. ↑) to AraC in relation to all samples in the wt<i>RAS</i> or mt<i>NRAS</i> cohort, respectively. Fisher`s exact test: p = 0.02. (C) Summary of the <i>in vitro</i> responses to AraC treatment in terms of differentiation of 22 primary AML blasts with or without FLT3-ITD. Fisher`s exact test: p = 0.19.</p

AML patient cohorts used in this study.

<p>GSEA: gene set enrichment analysis</p><p>AML patient cohorts used in this study.</p

AraC induces differentiation in the mt<i>NRAS</i> harboring AML cell line HL-60.

<p>(A) May-Grünwald-Giemsa staining of HL-60 and U937 (wt<i>RAS</i>) cells 48h after AraC treatment at indicated doses. (B) <i>CD14</i> expression in HL-60 and U937 cells 48 h after AraC-treatment at indicated doses as determined by quantitative real-time PCR. <i>GAPDH</i> was used for normalization. The graph shows the median with 95% confidence interval. Results were normalized to the respective control of each cell line. **: p = 0.002 (Student’s t-test).</p

Oncogenic <i>NRAS</i> Primes Primary Acute Myeloid Leukemia Cells for Differentiation

<div><p><i>RAS</i> mutations are frequently found among acute myeloid leukemia patients (AML), generating a constitutively active signaling protein changing cellular proliferation, differentiation and apoptosis. We have previously shown that treatment of AML patients with high-dose cytarabine is preferentially beneficial for those harboring oncogenic RAS. On the basis of a murine AML cell culture model, we ascribed this effect to a RAS-driven, p53-dependent induction of differentiation. Hence, in this study we sought to confirm the correlation between <i>RAS</i> status and differentiation of primary blasts obtained from AML patients. The gene expression signature of AML blasts with oncogenic <i>NRAS</i> indeed corresponded to a more mature profile compared to blasts with wildtype <i>RAS</i>, as demonstrated by gene set enrichment analysis (GSEA) and real-time PCR analysis of myeloid ecotropic viral integration site 1 homolog (<i>MEIS1</i>) in a unique cohort of AML patients. In addition, <i>in vitro</i> cell culture experiments with established cell lines and a second set of primary AML cells showed that oncogenic <i>NRAS</i> mutations predisposed cells to cytarabine (AraC) driven differentiation. Taken together, our findings show that AML with inv(16) and <i>NRAS</i> mutation have a differentiation gene signature, supporting the notion that <i>NRAS</i> mutation may predispose leukemic cells to AraC induced differentiation. We therefore suggest that promotion of differentiation pathways by specific genetic alterations could explain the superior treatment outcome after therapy in some AML patient subgroups. Whether a differentiation gene expression status may generally predict for a superior treatment outcome in AML needs to be addressed in future studies.</p></div

Impact of <i>NRAS</i> status on the transcriptome of primary AML blasts.

<p>(A-E) Enrichment plots as obtained by GSEA software for the gene sets CROONQUIST_NRAS_SIGNALING_UP, positive control; IVANOVA HEMATO-POIESIS_MATURE_CELL; JAATINEN_HEMATOPOIETIC_STEM _CELL _UP; BENPORATH_MYC_TARGETS_WITH_EBOX; IVANOVA_HEMATOPOIESIS_INTER-MEDIATE_PROGENITOR. Primary AML blasts harboring wt<i>NRAS</i> were compared with mt<i>NRAS</i> (12/13 or 61) blasts. (F) Relative expression of <i>MEIS1</i> in primary AML blasts carrying wt<i>RAS</i> or mt<i>NRAS</i> as examined by real-time PCR. The graph shows the median with 95% confidence interval. Results were normalized to <i>MEIS1</i> expression of mt<i>NRAS</i> blasts. <i>GAPDH</i> expression served as internal control. *: p = 0.025 (Mann Whitney test).</p

Plasma Synthesis of Carbon-Based Nanocarriers for Linker-Free Immobilization of Bioactive Cargo

Multifunctional nanoparticles are increasingly employed to improve biological efficiency in medical imaging, diagnostics, and treatment applications. However, even the most well-established nanoparticle platforms rely on multiple-step wet-chemistry approaches for functionalization often with linkers, substantially increasing complexity and cost, while limiting efficacy. Plasma dust nanoparticles are ubiquitous in space, commonly observed in reactive plasmas, and long regarded as detrimental to many manufacturing processes. As the bulk of research to date has sought to eliminate plasma nanoparticles, their potential in theranostics has been overlooked. Here we show that carbon-activated plasma-polymerized nanoparticles (nanoP³) can be synthesized in dusty plasmas with tailored properties, in a process that is compatible with scale up to high throughput, low-cost commercial production. We demonstrate that nanoP³ have a long active shelf life, containing a reservoir of long-lived radicals embedded during their synthesis that facilitate attachment of molecules upon contact with the nanoparticle surface. Following synthesis, nanoP³ are transferred to the bench, where simple one-step incubation in aqueous solution, without the need for intermediate chemical linkers or purification steps, immobilizes multiple cargo that retain biological activity. Bare nanoP³ readily enter multiple cell types and do not inhibit cell proliferation. Following functionalization with multiple fluorescently labeled cargo, nanoP³ retain their ability to cross the cell membrane. This paper shows the unanticipated potential of carbonaceous plasma dust for theranostics, facilitating simultaneous imaging and cargo delivery on an easily customizable, functionalizable, cost-effective, and scalable nanoparticle platform