Global temperature modes shed light on the Holocene temperature conundrum.

Reconstructions of the global mean annual temperature evolution during the Holocene yield conflicting results. One temperature reconstruction shows global cooling during the late Holocene. The other reconstruction reveals global warming.

Developments in the MPI-M Earth System Model version 1.2 (MPI-ESM1.2) and Its Response to Increasing CO.

A new release of the Max Planck Institute for Meteorology Earth System Model version 1.2 (MPI-ESM1.2) is presented.

Slowdown of the Walker circulation at solar cycle maximum.

The Pacific Walker Circulation (PWC) fluctuates on interannual and multidecadal timescales under the influence of internal variability and external forcings. Here, we provide observational evidence that the 11-y solar cycle (SC) affects the PWC on decadal timescales. We observe a robust reduction of east-west sea-level pressure gradients over the Indo-Pacific Ocean during solar maxima and the following 1-2 y.

Evaluating climate geoengineering proposals in the context of the Paris Agreement temperature goals.

Current mitigation efforts and existing future commitments are inadequate to accomplish the Paris Agreement temperature goals. In light of this, research and debate are intensifying on the possibilities of additionally employing proposed climate geoengineering technologies, either through atmospheric carbon dioxide removal or farther-reaching interventions altering the Earth's radiative energy budget. Although research indicates that several techniques may eventually have the physical potential to contribute to limiting climate change, all are in early stages of development, involve substantial uncertainties and risks, and raise ethical and governance dilemmas.

Mixed-Valent Molecular Triple Deckers.

Two phenothiazine (PTZ) moieties were connected via naphthalene spacers to a central arene to result in stacked PTZ-arene-PTZ structure elements. Benzene and tetramethoxybenzene units served as central arenes mediating electronic communication between the two PTZ units. Based on cyclic voltammetry, UV/Vis-NIR absorption, EPR spectroscopy, and computational studies, the one-electron oxidized forms of the resulting compounds behave as class II organic mixed-valence species in which the unpaired electron is partially delocalized over both PTZ units.

Electron Transfer around a Molecular Corner.

The distance dependence of electron transfer (ET) is commonly investigated in linear rigid rod-like compounds, but studies of molecular wires with integrated corners imposing 90° angles are very rare. By using spirobifluorene as a key bridging element and by substituting it at different positions, two isomeric series of donor-bridge-acceptor compounds with either nearly linear or angled geometries were obtained. Photoinduced ET in both series is dominated by rapid through-bond hole hopping across oligofluorene bridges over distances of up to 70 Å.

Transition to a Moist Greenhouse with CO2 and solar forcing.

Water-rich planets such as Earth are expected to become eventually uninhabitable, because liquid water turns unstable at the surface as temperatures increase with solar luminosity. Whether a large increase of atmospheric concentrations of greenhouse gases such as CO2 could also destroy the habitability of water-rich planets has remained unclear. Here we show with three-dimensional aqua-planet simulations that CO2-induced forcing as readily destabilizes the climate as does solar forcing.

Charge Transfer Pathways in Three Isomers of Naphthalene-Bridged Organic Mixed Valence Compounds.

Naphthalene was substituted at different positions with two identical triarylamine moieties to result in species which are mixed-valence compounds in their one-electron oxidized forms. They were investigated by cyclic voltammetry, optical absorption, EPR spectroscopy, X-ray crystallography, and DFT calculations. When the two redox-active triarylamine moieties are connected to the 2- and 6-positions of the naphthalene bridge, their electronic communication is significantly stronger than when they are linked to the 1- and 5-positions, and this can be understood on the basis of a simple through-bond charge transfer pathway model.

An economic evaluation of solar radiation management.

Economic evaluations of solar radiation management (SRM) usually assume that the temperature will be stabilized, with no economic impacts of climate change, but with possible side-effects. We know from experiments with climate models, however, that unlike emission control the spatial and temporal distributions of temperature, precipitation and wind conditions will change. Hence, SRM may have economic consequences under a stabilization of global mean temperature even if side-effects other than those related to the climatic responses are disregarded.

Multistage complexation of fluoride ions by a fluorescent triphenylamine bearing three dimesitylboryl groups: controlling intramolecular charge transfer.

A propeller-shaped boron-nitrogen compound (NB(3)) with three binding sites for fluoride anions was synthesized and investigated by optical absorption, luminescence, and ((1)H, (11)B, (13)C, (19)F) NMR spectroscopy. Binding of fluoride in dichloromethane solution occurs in three clearly identifiable steps and leads to stepwise blocking of the three initially present nitrogen-to-boron charge transfer pathways. As a consequence, the initially bright blue charge transfer emission is red-shifted and decreases in intensity, until it is quenched completely in presence of large fluoride excess.

CCR2+Ly-6Chi monocytes are crucial for the effector phase of autoimmunity in the central nervous system.

The chemokine receptor CCR2 plays a vital role for the induction of autoimmunity in the central nervous system. However, it remains unclear how the pathogenic response is mediated by CCR2-bearing cells. By combining bone marrow chimerism with gene targeting we detected a mild disease-modulating role of CCR2 during experimental autoimmune encephalomyelitis, a model for central nervous system autoimmunity, on radio-resistant cells that was independent from targeted CCR2 expression on endothelia.

Local type I IFN receptor signaling protects against virus spread within the central nervous system.

Several neurotropic viruses such as vesicular stomatitis virus (VSV) induce peripheral neutralizing Ab responses and still can infect cells within the CNS. To address whether local type I IFN receptor (IFNAR) triggering plays a role in controlling virus replication within the brain, we generated mice with a cell type-specific IFNAR deletion in neuroectodermal cells of the CNS (NesCre(+/-)IFNAR(flox/flox)). Intranasal VSV infection with 10(3) PFU was well tolerated by wild-type mice, whereas conventional IFNAR(-/-) mice died within 2-3 days.

Type I interferon receptor signalling is induced during demyelination while its function for myelin damage and repair is redundant.

The type I interferons, interferon-beta and alpha (IFN-beta, IFN-alpha), are widely used for the treatment of autoimmune demyelination in the central nervous system (CNS). Their effects on de- and remyelination through the broadly expressed type I IFN receptor (IFNAR), however, are highly speculative. In order to elucidate the role of endogenous type I interferons for myelin damage and recovery we induced toxic demyelination in the absence of IFNAR1.

Overexpression of lymphotoxin in T cells induces fulminant thymic involution.

Activated lymphocytes and lymphoid-tissue inducer cells express lymphotoxins (LTs), which are essential for the organogenesis and maintenance of lymphoreticular microenvironments. Here we describe that T-cell-restricted overexpression of LT induces fulminant thymic involution. This phenotype was prevented by ablation of the LT receptors tumor necrosis factor receptor (TNFR) 1 or LT beta receptor (LTbetaR), representing two non-redundant pathways.

Distinct and nonredundant in vivo functions of IFNAR on myeloid cells limit autoimmunity in the central nervous system.

The action of type I interferons in the central nervous system (CNS) during autoimmunity is largely unknown. Here, we demonstrate elevated interferon beta concentrations in the CNS, but not blood, of mice with experimental autoimmune encephalomyelitis (EAE), a model for CNS autoimmunity. Furthermore, mice devoid of the broadly expressed type I IFN receptor (IFNAR) developed exacerbated clinical disease accompanied by a markedly higher inflammation, demyelination, and lethality without shifting the T helper 17 (Th17) or Th1 cell immune response.

Microglia in the adult brain arise from Ly-6ChiCCR2+ monocytes only under defined host conditions.

Microglia are crucially important myeloid cells in the CNS and constitute the first immunological barrier against pathogens and environmental insults. The factors controlling microglia recruitment from the blood remain elusive and the direct circulating microglia precursor has not yet been identified in vivo. Using a panel of bone marrow chimeric and adoptive transfer experiments, we found that circulating Ly-6C(hi)CCR2(+) monocytes were preferentially recruited to the lesioned brain and differentiated into microglia.

Inhibition of transcription factor NF-kappaB in the central nervous system ameliorates autoimmune encephalomyelitis in mice.

Activation of transcription factor NF-kappaB in the central nervous system (CNS) has been linked to autoimmune demyelinating disease; however, it remains unclear whether its function is protective or pathogenic. Here we show that CNS-restricted ablation of 'upstream' NF-kappaB activators NEMO or IKK2 but not IKK1 ameliorated disease pathology in a mouse model of multiple sclerosis, suggesting that 'canonical' NF-kappaB activation in cells of the CNS has a mainly pathogenic function in autoimmune demyelinating disease. NF-kappaB inhibition prevented the expression of proinflammatory cytokines, chemokines and the adhesion molecule VCAM-1 from CNS-resident cells.

Circulating monocytes engraft in the brain, differentiate into microglia and contribute to the pathology following meningitis in mice.

Previous studies have demonstrated a potential role of brain endogenous microglia and meningeal macrophages in inflammation and brain injury during bacterial meningitis. However, the contribution of previously engrafted monocytes and microglia to this process is still unknown. We therefore used genetically labelled bone marrow-derived cells from transgenic mice expressing the green fluorescent protein (GFP) under the chicken beta-actin promoter to deliver fluorescently labelled monocytes to the diseased brain.

Streptococcus pneumoniae Infection aggravates experimental autoimmune encephalomyelitis via Toll-like receptor 2.

The course of autoimmune inflammatory diseases of the central nervous system (CNS) can be influenced by infections. Here we assessed the disease-modulating effects of the most frequent respiratory pathogen Streptococcus pneumonia on the course of experimental autoimmune encephalomyelitis (EAE). Mice were immunized with myelin oligodendrocyte glycoprotein 35-55 (MOG(35-55)) peptide, challenged intraperitoneally with live S.

Innate immunity mediated by TLR9 modulates pathogenicity in an animal model of multiple sclerosis.

Inflammatory diseases of the CNS, such as MS and its animal model EAE, are characterized by infiltration of activated lymphocytes and phagocytes into the CNS. Within the CNS, activation of resident cells initiates an inflammatory cascade, leading to tissue destruction, demyelination, and neurologic deficit. TLRs recognize microbes and are pivotal mediators of innate immunity.