Iron Oxide-Induced Thermal Effects on Solid-State Upconversion Emissions in NaYF₄:Yb,Er Nanocrystals

Multifunctional materials exhibiting photon upconversion show promising applications for biological imaging and sensing. In this study, we examine the solid-state upconversion emission of NaYF₄:Yb,Er nanoparticles in the presence of iron oxide nanoparticles. Fe₃O₄ nanoparticles (6 nm) were mixed with NaYF₄:Yb,Er nanoparticles (either 10 or 50 nm) in varying proportions by drying chloroform solutions of nanoparticles onto glass slides. Upconversion spectra were acquired, and a laser power-dependent emission was observed and correlated with the iron oxide content in the mixture. Changes in the lattice temperature of the upconverting particles were monitored by careful observation of the relative intensities of the ²H_11/2 and ⁴S_3/2 →⁴I_15/2 transitions. The emission characteristics observed are consistent with an iron oxide-induced thermal effect that is dependent on both the laser power and the proportion of iron oxide. The results highlight that the thermal effects of mixed nanoparticle systems should be considered in the design of luminescent upconverting hybrid materials

Proliferation of oligodendroglia subpopulations following partial ON transection.

<p>Oligodendroglia and other olig2+ glia were identified with antibodies to NG2 (A), olig2 (B) and Ki67 (C), or with CC1 (E), olig2 (F) and Ki67 (G). D: Cells indicated are Ki67+/NG2+/olig2+ (>) and Ki67−/NG2+/olig2+ (>>). H: Cells indicated are Ki67+/CC1+/olig2+ (>) and Ki67−/CC1+/olig2+ (>>). Proliferating Ki67+/IBA1+ cells (I, indicated by >) and to a lesser extent Ki67+/GFAP+ cells (J) were observed after injury; representative examples at 3 days shown. K–P: Quantification of the mean density ± S.E of oligodendroglia and other olig2+ glia populations following partial transection. Densities of Ki67– cells are represented by black bars while densities of Ki67+ cells are represented by red bars and differences from control indicated by Δ(p≤0.05). Overall differences in total density (combined Ki67+ and Ki67– values) compared to control are indicated by *(p≤0.05). Q: Summary graph of Ki67+ mean densities of all oligodendroglia and other olig2+ glia subpopulations. Scale bar A–H: 20 µm, I–J: 10 µm.</p

Oligodendroglia subpopulations of varying maturity in adult control ON.

<p>A: Schematic diagram illustrates changes in the expression of NG2 and CC1 markers, and olig2 transcription factor across oligodendroglia subpopulations <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0065710#pone.0065710-Nishiyama1" target="_blank">[24]</a>. Oligodendroglia and olig2+ glia were identified with combinations of antibodies to NG2 (B, D) and olig2 (C, D), or CC1 (E, G) and olig2 (F, G). D: Cells indicated are NG2+/olig2– (>), NG2+/olig2+ (>>) or NG2−/olig2+ (>l). G: Cells indicated are CC1+/olig2– (>) or CC1+/olig2+ (>>). H: Desmin+ cells (>) were not NG2+ (>>). Olig2 staining colocalises with Hoechst nuclear stain (I) and Nkx2.2+ nuclei (J). K: MBP+ myelin surrounds CC1+ oligodendrocyte somata. L: GFAP immunoreactivity surrounds some olig2+ nuclei (example >) but does not colocalise with CC1 (>>). M: Quantification of immunopositive oligodendroglia in control ON was expressed as the mean density of cells per mm² ± S.E. Scale bars: B–G: 20 µm, H–L: 10 µm.</p

Proportion of proliferating (Ki67+) cells that are immature oligodendroglia/CC1−/olig2+ glia.

<p>Data are expressed as percentages of the means ± SEM of data presented in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0065710#pone-0065710-g002" target="_blank">Figs. 2K–M</a>. Note that values do not sum to 100% due to over-lapping populations.</p

Myelin internode length following partial ON transection.

<p>Representative images of a single slice from the z stacks show ventral axons of control animals (A) and at 3 months following injury (B) anterogradely traced with CTB (green); paranodes are immunohistochemically labelled with Caspr and nodes with Nav1.6. C: The length of myelin internodes (indicated by <) under 110 µm were measured between paranodes (Caspr+ structures, red, confirmed by the presence of Nav1.6+ sodium channels, blue, at the node, indicated by brackets) and the data range, 25% and 75% percentile, median and mean (indicated by *) were displayed in the box plot. D: Mean number of internodes visible per FOV ± S.E (*p<0.05). Scale bar: 20 µm.</p

GSEA of differentially expressed genes (FC > 1.4, p-value < 0.05) between dorsal and ventral retina, showing GO classified biological_functions at day 1 and day 7 after PT injury.

<p>All biological_function clusters are upregulated in dorsal retina when compared to ventral retina. Top 10 significant (p-value < 0.05) biological_functions shown for day 1 with a list of contributing genes that are differentially expressed by fold change > 2, p-value < 0.05. Only 2 clusters were enriched from differentially expressed genes between dorsal and ventral retina at day 7 after injury. The genes listed are differentially expressed by a FC > 1.5. The bar graph depicts the total number of genes that contribute to each functional cluster.</p

Downregulated genes in dorsal and ventral retina following a PT injury.

<p>Fold changes comparing injured retina to region matched normal controls.</p

Une cloche sonnant la retraite nommée "Côparèye". Petit essai de campanonymie et de sémiologie campanaire

L'article propose l'étymologie du nom de la cloche la plus fameuse de la cathédrale Saint-Lambert de Liège et jette les bases d'une campanonymie (étude des noms de cloches) d'origine délocutive (mots tirant leur origine d'énoncés).Peer reviewe

Upregulated genes in dorsal and ventral retina following a PT injury.

<p>Fold changes comparing injured retina to region matched normal controls.</p

Discriminant analysis on biological clusters related to oxidation-reduction, immune response and apoptosis after partial optic nerve injury.

<p>Discriminant analysis on biological clusters related to oxidation-reduction, immune response and apoptosis after partial optic nerve injury.</p