Image_1_Topic modeling three decades of climate change news in Denmark.JPEG

Climate change is a dynamic and rapidly evolving media agenda. First associated with scientific notions of the greenhouse effect, it was later presented as global warming before reaching the current and broader picture of climate change. Over its development, climate change reporting has touched on a broad range of topics reflecting shifting scientific understandings, political interventions, and public anxieties, all of which condition the public's view and actions on climate change. To better understand which issues the Danish public has been exposed to, this study uses topic modeling to analyse 32 years of climate change communication in Denmark (1990–2021, n = 63,743). It identifies 85 topics grouped into 14 themes dealing with climate change in Danish national media outlets. Topics differ in prevalence and longitudinal stability while reflecting outlet bias in political leaning and communicative modalities. The most pronounced differences in climate change reporting are between public service media and traditional newspapers. This indicates that media users relying mainly on online news from public service providers, without additional access to print media, will receive information on climate change that is more topical and less politicized, more thematic and less structural, more about high-level politics than everyday interventions and more concerned with consequences than solutions.</p

Table_1_Topic modeling three decades of climate change news in Denmark.DOCX

Climate change is a dynamic and rapidly evolving media agenda. First associated with scientific notions of the greenhouse effect, it was later presented as global warming before reaching the current and broader picture of climate change. Over its development, climate change reporting has touched on a broad range of topics reflecting shifting scientific understandings, political interventions, and public anxieties, all of which condition the public's view and actions on climate change. To better understand which issues the Danish public has been exposed to, this study uses topic modeling to analyse 32 years of climate change communication in Denmark (1990–2021, n = 63,743). It identifies 85 topics grouped into 14 themes dealing with climate change in Danish national media outlets. Topics differ in prevalence and longitudinal stability while reflecting outlet bias in political leaning and communicative modalities. The most pronounced differences in climate change reporting are between public service media and traditional newspapers. This indicates that media users relying mainly on online news from public service providers, without additional access to print media, will receive information on climate change that is more topical and less politicized, more thematic and less structural, more about high-level politics than everyday interventions and more concerned with consequences than solutions.</p

Parallel Accumulation–Serial Fragmentation (PASEF): Multiplying Sequencing Speed and Sensitivity by Synchronized Scans in a Trapped Ion Mobility Device

In liquid chromatography-mass spectrometry (LC-MS)-based proteomics, many precursors elute from the column simultaneously. In data-dependent analyses, these precursors are fragmented one at a time, whereas the others are discarded entirely. Here we employ trapped ion mobility spectrometry (TIMS) on an orthogonal quadrupole time-of-flight (QTOF) mass spectrometer to remove this limitation. In TIMS, all precursor ions are accumulated in parallel and released sequentially as a function of their ion mobility. Instead of selecting a single precursor mass with the quadrupole mass filter, we here implement synchronized scans in which the quadrupole is mass positioned with sub-millisecond switching times at the <i>m</i>/<i>z</i> values of appropriate precursors, such as those derived from a topN precursor list. We demonstrate serial selection and fragmentation of multiple precursors in single 50 ms TIMS scans. Parallel accumulation–serial fragmentation (PASEF) enables hundreds of MS/MS events per second at full sensitivity. Modeling the effect of such synchronized scans for shotgun proteomics, we estimate that about a 10-fold gain in sequencing speed should be achievable by PASEF without a decrease in sensitivity

From Bis(silylene) and Bis(germylene) Pincer-Type Nickel(II) Complexes to Isolable Intermediates of the Nickel-Catalyzed Sonogashira Cross-Coupling Reaction

The first [ECE]­Ni­(II) pincer complexes with E = Si^II and E = Ge^II metallylene donor arms were synthesized via C–X (X = H, Br) oxidative addition, starting from the corresponding [EC­(X)­E] ligands. These novel complexes were fully characterized (NMR, MS, and XRD) and used as catalyst for Ni-catalyzed Sonogashira reactions. These catalysts allowed detailed information on the elementary steps of this catalytic reaction (transmetalation → oxidative addition → reductive elimination), resulting in the isolation and characterization of an unexpected intermediate in the transmetalation step. This complex, {[ECE]­Ni acetylide → CuBr} contains both nickel and copper, with the copper bound to the alkyne π-system. Consistent with these unusual structural features, DFT calculations of the {[ECE]­Ni acetylide → CuBr} intermediates revealed an unusual E–Cu–Ni three-center–two-electron bonding scheme. The results reveal a general reaction mechanism for the Ni-based Sonogashira coupling and broaden the application of metallylenes as strong σ-donor ligands for catalytic transformations

Synthesis, Reactivity, and Electronic Structure of a Bioinspired Heterobimetallic [Ni(μ‑S₂)Fe] Complex with Disulfur Monoradical character

The first synthesis of a monoradical Ni­(μ-S₂)­Fe core in the [(Nacnac)­Ni­(μ-S₂)­Fe­(dmpe)₂] complex <b>3</b> could be accomplished in good yields by PMe₃ elimination from the zerovalent iron complex [(dmpe)₂(PMe₃)­Fe] (<b>2</b>; dmpe =1,2-bis­(dimethylphosphine)­ethane) upon reaction with the supersulfido nickel­(II) complex [(Nacnac)­Ni­(S₂)] (<b>1</b>; Nacnac = CH­{(CMe)­(2,6-^<i>i</i>Pr₂C₆H₃N)}₂). Complex <b>3</b> bears Ni­(II) and Fe­(II) centers, both of which are in a low-spin state. A single electron is located in the HOMO and is somewhat delocalized over the Ni­(μ-S₂)Fe core, so that the bridging disulfur subunit exhibits some “subsulfide” S₂^3– character. Compound <b>3</b> represents a bioinspired example of a monoradical with a Ni­(μ-S₂)Fe structural motif, reminiscent of the Ni­(μ-S₂)Fe core structure of the active site in [NiFe] hydrogenases. Its oxidation with [Fe­(η⁵-C₅H₅)₂]­[B­(C₆H₃(CF₃)₂)₄] affords the product [(Nacnac)­Ni­(μ-S)₂Fe­(dmpe)₂]­[B­(C₆H₃(CF₃)₂)₄] (<b>4</b>), and complex <b>3</b> can alternatively be prepared via a reductive route upon reaction of [Co­(η⁵-C₅Me₅)₂]­[(Nacnac)­NiS₂] (<b>6</b>) with the Fe(0) precursor <b>2</b>. All synthesized complexes were fully characterized, including in some cases single-crystal X-ray diffraction analysis, magnetometry, EPR, NMR, and ⁵⁷Fe Mössbauer spectroscopy. DFT calculations were used to compute the spectroscopic parameters and to establish the electronic structure of <b>3</b> and its oxidized and reduced forms and related complexes

<i>Fgfr2</i> deficiency leads to locomotor deficits in adult mice.

<p>(<b>A–D</b>) Cresyl-violet stained brightfield (A,C) and darkfield (B,D) views of sagittal sections from adult <i>Fgfr2^lox/lox</i> (control, A,B) and <i>Nestin-Cre;Fgfr2^lox/lox</i> (<i>Fgfr2</i> cKO, C,D) cerebella, hybridized with a radioactive <i>Fgfr2 exon 5</i> riboprobe. (<b>E</b>) Western blotting detected the full-length FGFR2 protein (approx. 100 kD) in brain lysates of adult <i>Fgfr2^lox/lox</i> (c, control) and <i>Nestin-Cre;Fgfr2^+/lox</i> (het, heterozygote) but not <i>Nestin-Cre;Fgfr2^lox/lox</i> (hom, homozygote) mice. Hprt is the loading control. (<b>F–J</b>) Behavioral tests revealed an altered horizontal locomotion (maximum velocity (F) and total distance travelled (G)) and unsupported vertical locomotion (latency to first rearing (H) and number of rearings (I) on the board) of male <i>Fgfr2</i> cKO (blue squares; n = 12 males) compared with control (red circles; n = 15 males) mice in the modified hole board paradigm, but no significant differences between both genotypes in the accelerating Rotarod performance (measured by mean latency to fall, J). Values are given in Table S1. I-X, lobuli of the adult cerebellum; ChPl, choroid plexus. Scale bar (C): 500 µm.</p

FGF target gene activation is almost completely abolished in the CbA of <i>Fgfr2</i> cKO embryos.

<p>(<b>A–P</b>) Representative sagittal brightfield views of E16.5 (A–H; n = 5 embryos/genotype) and E18.5 (I-P; n = 4 embryos/genotype) control (A,C,E,G,I,K,M,O) and <i>Fgfr2</i> cKO (B,D,F,H,J,L,N,P) cerebella, hybridized with riboprobes for <i>Etv5</i> (A–D,I–L) and <i>Tnc</i> (E,F,M,N). (C,D) and (K,L) are higher magnifications of the boxed areas in (A,B) and (I,J), respectively. (G,H) and (O,P) are pseudo-colored overlays (<i>Etv5</i> in red, <i>Tnc</i> in green, overlapping expression domains appear in yellow) of the adjacent sections shown in (C–F) and (K–N), respectively. Red arrowheads in (D,F,L,N) point at ectopic <i>Etv5</i>⁺ (D,L) or <i>Tnc</i>⁺ (F,N) cells in the anterior EGL of the mutant embryos. Note that at E18.5, the ectopic <i>Etv5</i>⁺ cells are predominantly located in the outer margin of the EGL, whereas the ectopic <i>Tnc</i>⁺ cells are mostly confined to the inner EGL. EGL, external granular layer; PCL, Purkinje cell layer. Scale bars: 100 µm (B); 50 µm (H).</p

Disruption of the anterior PCL but apparently normal RG scaffold in the <i>Fgfr2</i> cKO CbA.

<p>(<b>A–N</b>) Representative confocal overviews (A,B,E,F) and close-up views (C,D,G–N) of the anterior CbA on sagittal sections from control (A,C,E,G,I,K,M) and <i>Fgfr2</i> cKO (B,D,F,H,J,L,N) embryos at E18.5 (n = 5 embryos/genotype), immunostained for Pax6 (cyan/green in A–D; a marker for GCPs) and Calb1 (red in A–D; a marker for PCs), or Ccnd1 (cyan/green in E–J; a marker for cycling GCPs and RG/BG precursors/cells) and Glast (red in E–H,K,L; a marker for RG/BG fibers), and counterstained with DAPI (blue in A–H,M,N; a nuclear marker). (C,D) and (G,H) are close-up views of the boxed areas in (A,B) and (E,F), respectively, (G,I,K,M) were taken from an adjacent section to the one shown in (E). (I–N) are single color channel views of (G,H), respectively. Yellow arrowheads in (D) delimit the lacking Calb1⁺ anterior PCL in the mutant embryos, and in (H,J) point at ectopically located Ccnd1⁺ RG/BG precursors within the mutant cerebellar VZ. White arrowheads in (H,J) delimit the distorted Ccnd1⁺ anterior outer EGL in the mutant embryos. EGL, external granular layer; PCL, Purkinje cell layer; VZ, cerebellar ventricular zone. Scale bars: 100 µm (A); 30 µm (C); 50 µm (E).</p

FGF9/FGFR signaling inhibits the migration of RG/BG precursors/cells in cerebellar microexplants <i>in vitro</i>.

<p>(<b>A</b>) Migration assays were performed with similarly sized (black dotted bars) CbA microexplants from E16.5 wild-type (CD-1) mice, containing Pax6⁺/Ccnd1⁺ GCPs in the outer EGL (yellow), Ccnd1⁺ RG/BG precursors and cells (green), Pax6⁺ postmitotic GCs and inner CbA cells (pink), and DAPI⁺ PCs (blue). ChPl, choroid plexus; EGL, external granular layer; IC, inferior colliculus; VZ, cerebellar ventricular zone. CbA microexplants were treated with control medium or medium containing 100 ng/ml FGF9 or 20 µM SU5402. The distance (d) migrated by each Pax6⁻/Ccnd1⁺ (green), Pax6⁺/Ccnd1⁺ (yellow) and Pax6⁺/Ccnd1⁻ (pink) cell from the border of the microexplant was measured after 36 h of incubation. (<b>B–D</b>) Representative confocal overviews of Ccnd1⁺ (green) and/or Pax6⁺ (red) cells (double-positive cells appear in yellow), counterstained with DAPI (blue) (overlays with single-positive cells appear in light green and pink, respectively), that migrated from the border of the CbA microexplant (white line) in control (B), FGF9- (C) or SU5402- (D) containing medium. Red arrowheads point at the front-most Ccnd1⁺/Pax6⁻ (green) cells. (<b>E</b>) Quantification of the average distance migrated by RG/BG precursors/cells (green bars) and GCPs (yellow bars) in control- (n = 8 explants), FGF9- (n = 8 explants) or SU5402- (n = 6 explants) treated microexplant cultures (Distance (µm): RG/BG precursors/cells, control, 86.2±16.8; +FGF9, 52.6±20.9; +SU5402, 89.3±33.2; GCPs, control, 111.7±15.3; +FGF9, 97.7±16.8; +SU5402, 100.2±15.6; one-way ANOVA). (<b>F</b>) Quantification of the proportion of Ccnd1⁺/Pax6⁻ RG/BG precursors/cells among the total number of migrating Ccnd1⁺ and/or Pax6⁺ cells in control-, FGF9- or SU5402-treated microexplant cultures (% Ccnd1⁺/Pax6⁻ RG/BG precursors/cells: control, 3.66, 95% confidence interval [2.95,4.48] (8 experiments for controls with 128–589 migrated cells, among them 2-29 RG/BG cells); +FGF9, 1.31, 95% confidence interval [0.84,1.92] (8 experiments for FGF9 with 79-501 migrated cells, among them 0–9 RG/BG cells); +SU5402, 2.89, 95% confidence interval [1.99,4.04] (6 experiments for SU5402 with 78–371 migrated cells, among them 0–15 RG/BG cells); <i>P</i>-values from contrasts of a logistic model). (<b>G</b>) Average proportions of Ccnd1⁺/Pax6⁻ RG/BG precursors/cells among the total number of migrating Ccnd1⁺ and/or Pax6⁺ cells in each 50-µm bin in control- (grey bars), FGF9- (red bars) or SU5402- (green bars) treated microexplant cultures were estimated with a logistic model. Values are given in Table S2 in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0101124#pone.0101124.s001" target="_blank">File S1</a>. Scale bar (D): 100 µm.</p

Reduced numbers and mispositioning of <i>Tnc</i>⁺ BG cells in the EGL of the <i>Fgfr2</i> cKO CbA.

<p>(<b>A–J</b>) Representative sagittal brightfield views of E16.5 (A–D, n = 4 embryos/genotype), E17.5 (E–H, n = 1 embryo/genotype) and E18.5 (I,J, n = 3 embryos/genotype) control (A,C,E,G,I) and <i>Fgfr2</i> cKO (B,D,F,H,J) cerebella hybridized with radioactive <i>Tnc</i> (A–F,I,J) and <i>Fgfr2</i> (G,H) riboprobes. (C,D) are higher magnifications of the boxed areas in (A,B). (E–H) are higher magnifications of the anterior CbA in adjacent sections from control or mutant embryos. Red arrowheads in (D,F) point at ectopically positioned <i>Tnc</i>⁺ BG cells in the mutant EGL. Note the complete absence of the <i>Fgfr2</i> ISH signal correlating with less <i>Tnc</i>⁺ and intensely Nissl-stained cells in the CbA of the <i>Fgfr2</i> cKO embryo shown in (F,H), although some <i>Fgfr2</i>⁺ cells are detected in the (non-neural) mesenchyme overlying the mutant EGL. Red dotted line in (A,I) delimits the anterior area used for quantification. (<b>K,L</b>) High magnification views of the EGL and PCL on adjacent sections from an E18.5 control (wild-type) embryo, hybridized with a radioactive riboprobe for <i>Fgfr2</i> (red in K) or <i>Tnc</i> (black in L). Black arrowheads point at intensely Nissl-stained cells showing an ISH signal for <i>Fgfr2</i> (K) or <i>Tnc</i> (L). Empty arrowheads point at larger, weakly Nissl-stained cells devoid of <i>Fgfr2</i> (K) or <i>Tnc</i> (L) ISH signals. (<b>M,N</b>) Quantification of <i>Tnc</i>⁺ cells in the anterior CbA (M) and EGL (N) of control (grey bars) and mutant (white bars) embryos at E16.5 and E18.5 (<i>Tnc</i>⁺ cells/µm² (M): E16.5: control, 6.49×10⁻⁴±2.5×10⁻⁵ (n = 4 embryos); <i>Fgfr2</i> cKO, 4.43×10⁻⁴±2.4×10⁻⁵ (n = 4 embryos); E18.5: control, 9.41×10⁻⁴±5.9×10⁻⁵ (n = 3 embryos); <i>Fgfr2</i> cKO, 6.25×10⁻⁴±5.6×10⁻⁵ (n = 3 embryos); <i>Tnc</i>⁺ cells in anterior EGL (N): E16.5: control, 3.00±0.41 (n = 4 embryos); <i>Fgfr2</i> cKO, 17.00±1.29 (n = 4 embryos); E18.5: control, 5.67±0.88 (n = 3 embryos); <i>Fgfr2</i> cKO, 13.33±2.33 (n = 3 embryos); Student's <i>t</i>-test). EGL, external granular layer; PCL, Purkinje cell layer; VZ, cerebellar ventricular zone. Scale bars: 100 µm (B); 50 µm (D,H); 30 µm (L).</p