Two triphenylamine‐based metal‐free organic sensitizers, D35 with a single anchor group and M14 with two anchor groups, have been applied in dye‐sensitized solar cells (DSCs) with a solid hole transporting material or liquid iodide/triiodide based electrolyte. Using the molecular hole conductor 2,2',7,7'‐tetrakis‐(N,N‐di‐p‐methoxyphenyl‐amine)9,9'‐spirobifluorene (spiro‐OMeTAD), good overall conversion efficiencies of 4.5% for D35 and 4.4% for M14 were obtained under standard AM 1.5G illumination (100 mW cm−2). Although M14 has a higher molar extinction coefficient (by ∼ 60%) and a slightly broader absorption spectrum compared to D35, the latter performs slightly better due to longer lifetime of electrons in the TiO2, which can be attributed to differences in the molecular structure. In iodide/triiodide electrolyte‐based DSCs, D35 outperforms M14 to a much greater extent, due to a very large increase in electron lifetime. This can be explained by both the greater blocking capability of the D35 monolayer and the smaller degree of interaction of triiodide (iodine) with D35 compared to M14. The present work gives some insight into how the molecular structure of sensitizer affects the performance in solid‐state and iodide/triiodide‐based DSCs.

Hard X-ray photoelectron spectroscopy (HAXPES) has been used to study the effects of adding Li-TFSI to hole conducting molecular thin films of 2,2′,7,7′-tetrakis(N,N′-di-p-methoxyphenylamine)-9,9′-spirobifluorene (spiro-OMeTAD). The work shows that a procedure of mixing a Li-TFSI solution into a spiro-OMeTAD solution, and subsequent spin-coating this mixture into a solid thin film causes the Fermi level of the molecular film to move closer to the HOMO level. Hence, adding the Li-TFSI gives similar effects to spiro-OMeTAD as a p-dopant. Specific effects from doping on the valence levels were also characterized. Absorbance measurements also showed that the spiro-OMeTAD film was partially oxidized when Li-TFSI was added before spin-coating. By varying the photon energy in the photoelectron spectroscopy measurements, the probe depth varies between being surface sensitive (<1 nm) and bulk sensitive (inelastic mean free path ≥10 nm). This property was used to follow differences in the composition at different depth of the spiro-OMeTAD/Li-TFSI film. It could be concluded that there was a concentration gradient in the molecular film and that the concentration of Li-TFSI was dominating at the interface between the spiro-OMeTAD/Li-TFSI film and vacuum.

International audienceMarine recreational fishing (MRF) is a high-participation activity with large economic value and social benefits globally, and it impacts on some fish stocks. Although reporting MRF catches is a European Union legislative requirement, estimates are only available for some countries. Here, data on numbers of fishers, participation rates, days fished, expenditures, and catches of two widely targeted species were synthesized to provide European estimates of MRF and placed in the global context. Uncertainty assessment was not possible due to incomplete knowledge of error distributions; instead, a semi-quantitative bias assessment was made. There were an estimated 8.7 million European recreational sea fishers corresponding to a participation rate of 1.6%. An estimated 77.6 million days were fished, and expenditure was €5.9 billion annually. There were higher participation, numbers of fishers, days fished and expenditure in the Atlantic than the Mediterranean, but the Mediterranean estimates were generally less robust. Comparisons with other regions showed that European MRF participation rates and expenditure were in the mid-range, with higher participation in Oceania and the United States, higher expenditure in the United States, and lower participation and expenditure in South America and Africa. For both northern European sea bass (Dicentrarchus labrax, Moronidae) and western Baltic cod (Gadus morhua, Gadidae) stocks, MRF represented 27% of the total removals. This study highlights the importance of MRF and the need for bespoke, regular and statistically sound data collection to underpin European fisheries management. Solutions are proposed for future MRF data collection in Europe and other regions to support sustainable fisheries management

Different somatic motor neuron subpopulations show a differential vulnerability to degeneration in diseases such as amyotrophic lateral sclerosis, spinal muscular atrophy and spinobulbar muscular atrophy. Studies in mutant superoxide dismutase 1 over-expressing amyotrophic lateral sclerosis model mice indicate that initiation of disease is intrinsic to motor neurons, while progression is promoted by astrocytes and microglia. Therefore, analysis of the normal transcriptional profile of motor neurons displaying differential vulnerability to degeneration in motor neuron disease could give important clues to the mechanisms of relative vulnerability. Global gene expression profiling of motor neurons isolated by laser capture microdissection from three anatomical nuclei of the normal rat, oculomotor/trochlear (cranial nerve 3/4), hypoglossal (cranial nerve 12) and lateral motor column of the cervical spinal cord, displaying differential vulnerability to degeneration in motor neuron disorders, identified enriched transcripts for each neuronal subpopulation. There were striking differences in the regulation of genes involved in endoplasmatic reticulum and mitochondrial function, ubiquitination, apoptosis regulation, nitrogen metabolism, calcium regulation, transport, growth and RNA processing; cellular pathways that have been implicated in motor neuron diseases. Confirmation of genes of immediate biological interest identified differential localization of insulin-like growth factor II, guanine deaminase, peripherin, early growth response 1, soluble guanylate cyclase 1A3 and placental growth factor protein. Furthermore, the cranial nerve 3/4-restricted genes insulin-like growth factor II and guanine deaminase protected spinal motor neurons from glutamate-induced toxicity (P < 0.001, ANOVA), indicating that our approach can identify factors that protect or make neurons more susceptible to degeneration.