1,512 research outputs found
Osedax borings in fossil marine bird bones
The bone-eating marine annelid Osedax consumes mainly whale bones on the deep-sea floor, but recent colonization experiments with cow bones and molecular age estimates suggesting a possible Cretaceous origin of Osedax indicate that this worm might be able grow on a wider range of substrates. The suggested Cretaceous origin was thought to imply that Osedax could colonize marine reptile or fish bones, but there is currently no evidence that Osedax consumes bones other than those of mammals. We provide the first evidence that Osedax was, and most likely still is, able to consume non-mammalian bones, namely bird bones. Borings resembling those produced by living Osedax were found in bones of early Oligocene marine flightless diving birds (family Plotopteridae). The species that produced these boreholes had a branching filiform root that grew to a length of at least 3 mm, and lived in densities of up to 40 individuals per square centimeter. The inclusion of bird bones into the diet of Osedax has interesting implications for the recent suggestion of a Cretaceous origin of this worm because marine birds have existed continuously since the Cretaceous. Bird bones could have enabled this worm to survive times in the Earth’s history when large marine vertebrates other than fish were rare, specifically after the disappearance of large marine reptiles at the end-Cretaceous mass extinction event and before the rise of whales in the Eocene
Modified Zakharov equations for plasmas with a quantum correction
Quantum Zakharov equations are obtained to describe the nonlinear interaction
between quantum Langmuir waves and quantum ion-acoustic waves. These quantum
Zakharov equations are applied to two model cases, namely the four-wave
interaction and the decay instability. In the case of the four-wave
instability, sufficiently large quantum effects tend to suppress the
instability. For the decay instability, the quantum Zakharov equations lead to
results similar to those of the classical decay instability except for quantum
correction terms in the dispersion relations. Some considerations regarding the
nonlinear aspects of the quantum Zakharov equations are also offered.Comment: 4 figures. Accepted for publication in Physics of Plasmas (2004
Novel tau filament fold in chronic traumatic encephalopathy encloses hydrophobic molecules
Chronic traumatic encephalopathy (CTE) is a neurodegenerative tauopathy that is associated with repetitive head impacts or exposure to blast waves. First described as punch-drunk syndrome and dementia pugilistica in retired boxers1-3, CTE has since been identified in former participants of other contact sports, ex-military personnel and after physical abuse4-7. No disease-modifying therapies currently exist, and diagnosis requires an autopsy. CTE is defined by an abundance of hyperphosphorylated tau protein in neurons, astrocytes and cell processes around blood vessels8,9. This, together with the accumulation of tau inclusions in cortical layers II and III, distinguishes CTE from Alzheimer's disease and other tauopathies10,11. However, the morphologies of tau filaments in CTE and the mechanisms by which brain trauma can lead to their formation are unknown. Here we determine the structures of tau filaments from the brains of three individuals with CTE at resolutions down to 2.3 Å, using cryo-electron microscopy. We show that filament structures are identical in the three cases but are distinct from those of Alzheimer's and Pick's diseases, and from those formed in vitro12-15. Similar to Alzheimer's disease12,14,16-18, all six brain tau isoforms assemble into filaments in CTE, and residues K274-R379 of three-repeat tau and S305-R379 of four-repeat tau form the ordered core of two identical C-shaped protofilaments. However, a different conformation of the β-helix region creates a hydrophobic cavity that is absent in tau filaments from the brains of patients with Alzheimer's disease. This cavity encloses an additional density that is not connected to tau, which suggests that the incorporation of cofactors may have a role in tau aggregation in CTE. Moreover, filaments in CTE have distinct protofilament interfaces to those of Alzheimer's disease. Our structures provide a unifying neuropathological criterion for CTE, and support the hypothesis that the formation and propagation of distinct conformers of assembled tau underlie different neurodegenerative diseases
The novel MAPT mutation K298E:mechanisms of mutant tau toxicity, brain pathology and tau expression in induced fibroblast-derived neurons
Frontotemporal lobar degeneration (FTLD) consists of a group of neurodegenerative diseases characterized by behavioural and executive impairment, language disorders and motor dysfunction. About 20-30 % of cases are inherited in a dominant manner. Mutations in the microtubule-associated protein tau gene (MAPT) cause frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17T). Here we report a novel MAPT mutation (K298E) in exon 10 in a patient with FTDP-17T. Neuropathological studies of post-mortem brain showed widespread neuronal loss and gliosis and abundant deposition of hyperphosphorylated tau in neurons and glia. Molecular studies demonstrated that the K298E mutation affects both protein function and alternative mRNA splicing. Fibroblasts from a skin biopsy of the proband taken at post-mortem were directly induced into neurons (iNs) and expressed both 3-repeat and 4-repeat tau isoforms. As well as contributing new knowledge on MAPT mutations in FTDP-17T, this is the first example of the successful generation of iNs from skin cells retrieved post-mortem
On the linearization of the generalized Ermakov systems
A linearization procedure is proposed for Ermakov systems with frequency
depending on dynamic variables. The procedure applies to a wide class of
generalized Ermakov systems which are linearizable in a manner similar to that
applicable to usual Ermakov systems. The Kepler--Ermakov systems belong into
this category but others, more generic, systems are also included
Anisotropic Bose-Einstein condensates and completely integrable dynamical systems
A Gaussian ansatz for the wave function of two-dimensional harmonically
trapped anisotropic Bose-Einstein condensates is shown to lead, via a
variational procedure, to a coupled system of two second-order, nonlinear
ordinary differential equations. This dynamical system is shown to be in the
general class of Ermakov systems. Complete integrability of the resulting
Ermakov system is proven. Using the exact solution, collapse of the condensate
is analyzed in detail. Time-dependence of the trapping potential is allowed
Distribuição de fósforo no solo em razão do sistema de cultivo e manejo da adubação fosfatada.
Lie symmetries for two-dimensional charged particle motion
We find the Lie point symmetries for non-relativistic two-dimensional charged
particle motion. These symmetries comprise a quasi-invariance transformation, a
time-dependent rotation, a time-dependent spatial translation and a dilation.
The associated electromagnetic fields satisfy a system of first-order linear
partial differential equations. This system is solved exactly, yielding four
classes of electromagnetic fields compatible with Lie point symmetries
Silver staining (Campbell-Switzer) of neuronal α-synuclein assemblies induced by multiple system atrophy and Parkinson's disease brain extracts in transgenic mice.
Synucleinopathies [Parkinson's disease (PD), dementia with Lewy bodies (DLB) and multiple system atrophy (MSA)] share filamentous α-synuclein assemblies in nerve cells and glial cells. We compared the abilities of brain extracts from MSA and PD patients to induce neuronal α-synuclein assembly and neurodegeneration following intracerebral injection in heterozygous mice transgenic for human mutant A53T α-synuclein. MSA extracts were more potent than PD extracts in inducing α-synuclein assembly and in causing neurodegeneration. MSA assemblies were Campbell-Switzer- and Gallyas-silver-positive, whereas PD assemblies were only Campbell-Switzer-positive, in confirmation of previous findings. However, induced α-synuclein inclusions were invariably Campbell-Switzer-positive and Gallyas-negative, irrespective of whether MSA or PD brain extracts were injected. The α-synuclein inclusions of non-injected homozygous mice transgenic for A53T α-synuclein were also Campbell-Switzer-positive and Gallyas-negative. These findings demonstrate that transgene expression and its intracellular environment dominated over the silver staining properties of the conformers of assembled α-synuclein
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