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I sommeren 2022 har vi kortlagt Eskilsøs biodiversitet for at kunne dokumentere biodiversitetens fremtidige udvikling. Ynglefugle, planter, gødningsbiller, sommerfugle og bier er undersøgt samt kulstofindhold i jord – det sidste for at dokumentere ændringer i kulstoflagring ved ændret forvaltning. Øen er præget af tidligere dyrkning, og de største biodiversitetsværdier er de ynglende fugle og strandengene, som har et meget naturligt præg. Vi anbefaler at genoprette naturlig næringsstatus på tidligere dyrkningsflader, fx ved at afskrælle topjord, at igangsætte naturlig succession og græsning ved helårsgræsning med heste og okser. Vi anbefaler, at man undersøger muligheden for at skabe mere naturlig hydrologi ved at fjerne diget og evt. lade dele stå tilbage som ”fugleøer”. Genopretning af et naturligt økosystem kan være et forvaltningsmål i sig selv, men det vil indebære, at bekæmpelse af ræve ophører, og at naturlig prædation tillades. Desuden igangsættes genopretning af græsning med svin, som kan bidrage med forstyrrelser i jorden. Dog vil begge disse tiltag sandsynligvis påvirke jordrugende fugle negativt, og det skal derfor undersøges, om det i så fald vil være i strid med udpegningsgrundlaget.

We explore whether the integration of carbon offsets into investment portfolios improves perfor-mance. Our results show that investment strategies that include such offsets achieve higher Sharpe Ratios than the diversified benchmark portfolios. The efficient frontier of optimal portfolio choices is shifted upwards as a result of including compliance and voluntary carbon offsets in the portfolio. Our results also show that while diversified portfolios may benefit from carbon offsets integration, voluntary carbon offsets are significantly more sensitive to exogenous shocks than compliance carbon allowances. All these results are novel and may encourage investors to invest in such sustainable asset classes.

Additional file 1.

The synthesis and the first structural characterization of the halogenated pyridinium salts [C 5 F 5 NH] + , [C 5 F 4 ClNH] + , [(C 5 F 5 N) 2 H] + , [(C 5 Cl 5 N) 2 H] + of the weakly coordinating anion (WCA) [Al(OTeF 5 ) 4 ] − , showing noncovalent interactions in the solid state, are presented. The salts were characterized by the multinuclear NMR and IR spectroscopy as well as X-Ray diffraction. Hirshfeld surface analysis and solid state structures reveal various intermolecular anion-π and σ-hole interactions between the corresponding halogenated pyridinium cations and the anion [Al(OTeF 5 ) 4 ] − .

Glia are critical players in defining synaptic contacts and maintaining neuronal homeostasis. Both astrocytes as glia of the central nervous system (CNS), as well as satellite glial cells (SGC) as glia of the peripheral nervous system (PNS), intimately interact with microglia, especially under pathological conditions when glia regulate degenerative as well as regenerative processes. The chemotherapeutic agent paclitaxel evokes peripheral neuropathy and cognitive deficits; however, the mechanisms underlying these diverse clinical side effects are unclear. We aimed to elucidate the direct effects of paclitaxel on the function of astrocytes, microglia, and SGCs, and their glia-glia and neuronal-glia interactions. After intravenous application, paclitaxel was present in the dorsal root ganglia of the PNS and the CNS of rodents. In vitro, SGC enhanced the expression of pro-inflammatory factors and reduced the expression of neurotrophic factor NT-3 upon exposure to paclitaxel, resulting in predominantly neurotoxic effects. Likewise, paclitaxel induced a switch towards a pro-inflammatory phenotype in microglia, exerting neurotoxicity. In contrast, astrocytes expressed neuroprotective markers and increasingly expressed S100A10 after paclitaxel exposure. Astrocytes, and to a lesser extent SGCs, had regulatory effects on microglia independent of paclitaxel exposure. Data suggest that paclitaxel differentially modulates glia cells regarding their (neuro-) inflammatory and (neuro-) regenerative properties and also affects their interaction. By elucidating those processes, our data contribute to the understanding of the mechanistic pathways of paclitaxel-induced side effects in CNS and PNS.Keywords: paclitaxel, chemotherapy-related neurotoxicity, neuroinflammation, astrocytes, microglia, satellite glia cells, neural stem cells, BDNF (brain derived neurotrophic factor)