Oceanic loading of wildfire-derived organic compounds from a small mountainous river

Copyright 2008 by the American Geophysical Union.Small mountainous rivers (SMRs) export substantial amounts of sediment into the world's oceans. The concomitant yield of organic carbon (OC) associated with this class of rivers has also been shown to be significant and compositionally unique. We report here excessively high loadings of polycyclic aromatic hydrocarbons (PAHs), lignin, and levoglucosan, discharged from the Santa Clara River into the Santa Barbara Channel. The abundance of PAHs, levoglucosan, and lignin in Santa Barbara Channel sediments ranged from 201.7 to 1232.3 ng gdw−1, 1.3 to 6.9 μg gdw−1, and 0.3 to 2.2 mg per 100 mg of the sedimentary OC, respectively. Assuming a constant rate of sediment accumulation, the annual fluxes of PAHs, levoglucosan, and lignin, to the Santa Barbara Channel were respectively, 885.5 ± 170.2 ng cm−2 a−1, 3.5 ± 1.9 μg cm−2 a−1 and 1.4 ± 0.3 mg per 100 mg OC cm−2 a−1, over ∼30 years. The close agreement between PAHs, levoglucosan, and lignin abundance suggests that the depositional flux of these compounds is largely biomass combustion-derived. To that end, use of the Santa Clara River as a model for SMRs suggests this class of rivers may be one of the largest contributors of pyrolyzed carbon to coastal systems and the open ocean. Wildfire associated carbon discharged from other high yield fluvial systems, when considered collectively, may be a significant source of lignin, pyrolytic PAHs, and other pyrogenic compounds to the ocean. Extrapolating these methods over geologic time may offer useful historical information about carbon sequestration and burial in coastal sediments and affect coastal carbon budgets

The PIPER survey. II. The globular cluster systems of low surface brightness galaxies in the Perseus cluster

We present Hubble Space Telescope ACS/WFC and WFC3/UVIS imaging for a sample of 50 low-surface brightness (LSB) galaxies in the ∼ 1015 M☉ Perseus cluster, which were originally identified in ground-based imaging. We measure the structural properties of these galaxies and estimate the total number of globular clusters (GCs) they host. Around half of our sample galaxies meet the strict definition of an ultra-diffuse galaxy (UDG), while the others are UDG-like but are either somewhat more compact or slightly brighter. A small number of galaxies reveal systems with many tens of GCs, rivalling some of the richest GC systems known around UDGs in the Coma cluster. We find the sizes of rich GC systems, in terms of their half-number radii, extending to ∼1.2 times the half-light radii of their host galaxy on average. The mean colours of the GC systems are the same, within the uncertainties, as those of their host galaxy stars. This suggests that GCs and galaxy field stars may have formed at the same epoch from the same enriched gas. It may also indicate a significant contribution from disrupted GCs to the stellar component of the host galaxy as might be expected in the ‘failed galaxy’ formation scenario for UDGs

Chronic treatment with 17-DMAG improves balance and coordination in a new mouse model of Machado-Joseph disease

Machado-Joseph disease (MJD) or spinocerebellar ataxia type 3 (SCA3) is a neurodegenerative disease currently with no treatment. We describe a novel mouse model of MJD which expresses mutant human ataxin-3 at near endogenous levels and manifests MJD-like motor symptoms that appear gradually and progress over time. CMVMJD135 mice show ataxin-3 intranuclear inclusions in the CNS and neurodegenerative changes in key disease regions, such as the pontine and dentate nuclei. Hsp90 inhibition has shown promising outcomes in some neurodegenerative diseases, but nothing is known about its effects in MJD. Chronic treatment of CMVMJD mice with Hsp90 inhibitor 17-DMAG resulted in a delay in the progression of their motor coordination deficits and, at 22 and 24 weeks of age, was able to rescue the uncoordination phenotype to wild-type levels; in parallel, a reduction in neuropathology was observed in treated animals. We observed limited induction of heat-shock proteins with treatment, but found evidence that 17-DMAG may be acting through autophagy, as LC3-II (both at mRNA and protein levels) and beclin-1 were induced in the brain of treated animals. This resulted in decreased levels of the mutant ataxin-3 and reduced intranuclear aggregation of this protein. Our data validate this novel mouse model as a relevant tool for the study of MJD pathogenesis and for pre-clinical studies, and show that Hsp90 inhibition is a promising therapeutic strategy for MJD.We would like to thank to Dr. Henry Paulson for providing the anti-ataxin-3 serum, Dr. Monica Sousa for the pCMV vector and to Eng. Lucilia Goreti Pinto, Lu s Martins, Miguel Carneiro and Celina Barros for technical assistance. This work was supported by Fundacao para a Ciencia e Tecnologia through the projects FEDER/FCT, POCI/SAU-MMO/60412/2004 and PTDC/SAU-GMG/64076/2006. This work was supported by Fundacao para a Ciencia e Tecnologia through fellowships SFRH/BPD/91562/2012 to A.S-F., SFRH/BD/78388/2011 to S. D-S., SFRH/BD/51059/2010 to A.N-C., and SFRH/BPD/79469/2011 to A.T-C.

The disruption of proteostasis in neurodegenerative diseases

Cells count on surveillance systems to monitor and protect the cellular proteome which, besides being highly heterogeneous, is constantly being challenged by intrinsic and environmental factors. In this context, the proteostasis network (PN) is essential to achieve a stable and functional proteome. Disruption of the PN is associated with aging and can lead to and/or potentiate the occurrence of many neurodegenerative diseases (ND). This not only emphasizes the importance of the PN in health span and aging but also how its modulation can be a potential target for intervention and treatment of human diseases.info:eu-repo/semantics/publishedVersio

The Eta Chamaeleontis Cluster: Origin in the Sco-Cen OB Association

A young, nearby compact aggregate of X-ray emitting pre-main sequence stars was recently discovered in the vicinity of eta Cha (B8V). In this paper, we further investigate this cluster: its membership, its environs and origins. ROSAT HRI X-ray data for the cluster's T Tauri stars show high levels of magnetic activity and variability. The cluster has an anomalous X-ray luminosity function compared to other young clusters, deficient in stars with low, but detectable X-ray luminosities. This suggests that many low-mass members have escaped the surveyed core region. Photographic photometry from the USNO-A2.0 catalog indicates that additional, X-ray-quiet members exist in the cluster core region. The components of the eclipsing binary RS Cha, previously modeled in the literature as post-MS with discordant ages, are shown to be consistent with being coeval pre-MS stars. We compute the Galactic motion of the cluster from Hipparcos data, and compare it to other young stars and associations in the fourth Galactic quadrant. The kinematic study shows that the eta Cha cluster, the TW Hya association, and a new group near epsilon Cha, probably originated near the giant molecular cloud complex that formed the two oldest subgroups of the Sco-Cen OB association roughly 10-15 Myr ago. Their dispersal is consistent with the velocity dispersions seen in giant molecular clouds. A large H I filament and dust lane located near eta Cha has been identified as part of a superbubble formed by Sco-Cen OB winds and supernova remnants. The passage of the superbubble may have terminated star-formation in the eta Cha cluster and dispersed its natal molecular gas.Comment: 26 pages, 9 figures, LaTex2.09, ApJ, in press, http://etacha.as.arizona.edu/~eem/etacha/MLF00/index.htm

An astrocyte-dependent mechanism for neuronal rhythmogenesis

Communication between neurons rests on their capacity to change their firing pattern to encode different messages. For several vital functions, such as respiration and mastication, neurons need to generate a rhythmic firing pattern. Here we show in the rat trigeminal sensori-motor circuit for mastication that this ability depends on regulation of the extracellular Ca2+ concentration ([Ca2+]e) by astrocytes. In this circuit, astrocytes respond to sensory stimuli that induce neuronal rhythmic activity, and their blockade with a Ca2+ chelator prevents neurons from generating a rhythmic bursting pattern. This ability is restored by adding S100b, an astrocytic Ca2+-binding protein, to the extracellular space, while application of an anti-S100b antibody prevents generation of rhythmic activity. These results indicate that astrocytes regulate a fundamental neuronal property: the capacity to change firing pattern. These findings may have broad implications for many other neural networks whose functions depend on the generation of rhythmic activity

Audio-Visual Speech Timing Sensitivity Is Enhanced in Cluttered Conditions

Events encoded in separate sensory modalities, such as audition and vision, can seem to be synchronous across a relatively broad range of physical timing differences. This may suggest that the precision of audio-visual timing judgments is inherently poor. Here we show that this is not necessarily true. We contrast timing sensitivity for isolated streams of audio and visual speech, and for streams of audio and visual speech accompanied by additional, temporally offset, visual speech streams. We find that the precision with which synchronous streams of audio and visual speech are identified is enhanced by the presence of additional streams of asynchronous visual speech. Our data suggest that timing perception is shaped by selective grouping processes, which can result in enhanced precision in temporally cluttered environments. The imprecision suggested by previous studies might therefore be a consequence of examining isolated pairs of audio and visual events. We argue that when an isolated pair of cross-modal events is presented, they tend to group perceptually and to seem synchronous as a consequence. We have revealed greater precision by providing multiple visual signals, possibly allowing a single auditory speech stream to group selectively with the most synchronous visual candidate. The grouping processes we have identified might be important in daily life, such as when we attempt to follow a conversation in a crowded room

Splice Isoforms of the Polyglutamine Disease Protein Ataxin-3 Exhibit Similar Enzymatic yet Different Aggregation Properties

Protein context clearly influences neurotoxicity in polyglutamine diseases, but the contribution of alternative splicing to this phenomenon has rarely been investigated. Ataxin-3, a deubiquitinating enzyme and the disease protein in SCA3, is alternatively spliced to encode either a C-terminal hydrophobic stretch or a third ubiquitin interacting motif (termed 2UIM and 3UIM isoforms, respectively). In light of emerging insights into ataxin-3 function, we examined the significance of this splice variation. We confirmed neural expression of several minor 5′ variants and both of the known 3′ ataxin-3 splice variants. Regardless of polyglutamine expansion, 3UIM ataxin-3 is the predominant isoform in brain. Although 2UIM and 3UIM ataxin-3 display similar in vitro deubiquitinating activity, 2UIM ataxin-3 is more prone to aggregate and more rapidly degraded by the proteasome. Our data demonstrate how alternative splicing of sequences distinct from the trinucleotide repeat can alter properties of the encoded polyglutamine disease protein and thereby perhaps contribute to selective neurotoxicity

In Vivo Generation of Neurotoxic Prion Protein: Role for Hsp70 in Accumulation of Misfolded Isoforms

Prion diseases are incurable neurodegenerative disorders in which the normal cellular prion protein (PrPC) converts into a misfolded isoform (PrPSc) with unique biochemical and structural properties that correlate with disease. In humans, prion disorders, such as Creutzfeldt-Jakob disease, present typically with a sporadic origin, where unknown mechanisms lead to the spontaneous misfolding and deposition of wild type PrP. To shed light on how wild-type PrP undergoes conformational changes and which are the cellular components involved in this process, we analyzed the dynamics of wild-type PrP from hamster in transgenic flies. In young flies, PrP demonstrates properties of the benign PrPC; in older flies, PrP misfolds, acquires biochemical and structural properties of PrPSc, and induces spongiform degeneration of brain neurons. Aged flies accumulate insoluble PrP that resists high concentrations of denaturing agents and contains PrPSc-specific conformational epitopes. In contrast to PrPSc from mammals, PrP is proteinase-sensitive in flies. Thus, wild-type PrP rapidly converts in vivo into a neurotoxic, protease-sensitive isoform distinct from prototypical PrPSc. Next, we investigated the role of molecular chaperones in PrP misfolding in vivo. Remarkably, Hsp70 prevents the accumulation of PrPSc-like conformers and protects against PrP-dependent neurodegeneration. This protective activity involves the direct interaction between Hsp70 and PrP, which may occur in active membrane microdomains such as lipid rafts, where we detected Hsp70. These results highlight the ability of wild-type PrP to spontaneously convert in vivo into a protease-sensitive isoform that is neurotoxic, supporting the idea that protease-resistant PrPSc is not required for pathology. Moreover, we identify a new role for Hsp70 in the accumulation of misfolded PrP. Overall, we provide new insight into the mechanisms of spontaneous accumulation of neurotoxic PrP and uncover the potential therapeutic role of Hsp70 in treating these devastating disorders