Enrichment of the HR 8799 planets by minor bodies and dust

Context. In the Solar System, minor bodies and dust deliver various materials to planetary surfaces. Several exoplanetary systems are known to host inner and outer belts, analogues of the main asteroid belt and the Kuiper belt, respectively. Aims: We study the possibility that exominor bodies and exodust deliver volatiles and refractories to the exoplanets in the well-characterised system HR 8799. Methods: We performed N-body simulations to study the impact rates of minor bodies in the system HR 8799. The model consists of the host star, four giant planets (HR 8799 e, d, c, and b), 650 000 test particles representing the inner belt, and 1 450 000 test particles representing the outer belt. Moreover we modelled dust populations that originate from both belts. Results: Within a million years, the two belts evolve towards the expected dynamical structure (also derived in other works), where mean-motion resonances with the planets carve the analogues of Kirkwood gaps. We find that, after this point, the planets suffer impacts by objects from the inner and outer belt at rates that are essentially constant with time, while dust populations do not contribute significantly to the delivery process. We convert the impact rates to volatile and refractory delivery rates using our best estimates of the total mass contained in the belts and their volatile and refractory content. Over their lifetime, the four giant planets receive between 10-4 and 10-3 M⊕ of material from both belts. Conclusions: The total amount of delivered volatiles and refractories, 5 × 10-3 M⊕, is small compared to the total mass of the planets, 11 × 103 M⊕. However, if the planets were formed to be volatile-rich, their exogenous enrichment in refractory material may well be significant and observable, for example with JWST-MIRI. If terrestrial planets exist within the snow line of the system, volatile delivery would be an important astrobiological mechanism and may be observable as atmospheric trace gases

Enrichment of the HR 8799 planets by minor bodies and dust

In the Solar System, minor bodies and dust deliver various materials to planetary surfaces. Several exoplanetary systems are known to host inner and outer belts, analogues of the main asteroid belt and the Kuiper belt. We study the possibility that exominor bodies and exodust deliver volatiles and refractories to the exoplanets in the system HR8799 by performing N-body simulations. The model consists of the host star, four giant planets (HR8799 e, d, c, and b), 650000 test particles representing the inner belt, and 1450000 test particles representing the outer belt. Moreover we modelled dust populations that originate from both belts. Within a million years, the two belts evolve towards the expected dynamical structure (also derived in other works), where mean-motion resonances with the planets carve the analogues of Kirkwood gaps. We find that, after this point, the planets suffer impacts by objects from the inner and outer belt at rates that are essentially constant with time, while dust populations do not contribute significantly to the delivery process. We convert the impact rates to volatile and refractory delivery rates using our best estimates of the total mass contained in the belts and their volatile and refractory content. Over their lifetime, the four giant planets receive between $10^{-4}$ and 10^{-3}M_\bigoplus of material from both belts. The total amount of delivered volatiles and refractories, {5\times10^{-3}\textrm{M}_\bigoplus}, is small compared to the total mass of the planets, 11\times10^{3}\textrm{M}_\bigoplus. However, if the planets were formed to be volatile-rich, their exogenous enrichment in refractory material may well be significant and observable, for example with JWST-MIRI. If terrestrial planets exist within the snow line of the system, volatile delivery would be an important astrobiological mechanism and may be observable as atmospheric trace gases.Comment: 11 pages, 8 figures, accepted for publication in Astronomy&Astrophysic

Schizophrenia as a disorder of disconnectivity

Schizophrenia is considered as a neurodevelopmental disorder with genetic and environmental factors playing a role. Animal models show that developmental hippocampal lesions are causing disconnectivity of the prefrontal cortex. Magnetic resonance imaging and postmortem investigations revealed deficits in the temporoprefrontal neuronal circuit. Decreased oligodendrocyte numbers and expression of oligodendrocyte genes and synaptic proteins may contribute to disturbances of micro- and macro-circuitry in the pathophysiology of the disease. Functional connectivity between cortical areas can be investigated with high temporal resolution using transcranial magnetic stimulation (TMS), electroencephalography (EEG), and magnetoencephalography (MEG). In this review, disconnectivity between different cortical areas in schizophrenia patients is described. The specificity and the neurobiological origin of these connectivity deficits and the relation to the symptom complex of schizophrenia and the glutamatergic and GABAergic system are discussed

Blockade of Gap Junction Hemichannel Suppresses Disease Progression in Mouse Models of Amyotrophic Lateral Sclerosis and Alzheimer's Disease

Glutamate released by activated microglia induces excitotoxic neuronal death, which likely contributes to non-cell autonomous neuronal death in neurodegenerative diseases, including amyotrophic lateral sclerosis and Alzheimer's disease. Although both blockade of glutamate receptors and inhibition of microglial activation are the therapeutic candidates for these neurodegenerative diseases, glutamate receptor blockers also perturbed physiological and essential glutamate signals, and inhibitors of microglial activation suppressed both neurotoxic/neuroprotective roles of microglia and hardly affected disease progression. We previously demonstrated that activated microglia release a large amount of glutamate specifically through gap junction hemichannel. Hence, blockade of gap junction hemichannel may be potentially beneficial in treatment of neurodegenerative diseases.In this study, we generated a novel blood-brain barrier permeable gap junction hemichannel blocker based on glycyrrhetinic acid. We found that pharmacologic blockade of gap junction hemichannel inhibited excessive glutamate release from activated microglia in vitro and in vivo without producing notable toxicity. Blocking gap junction hemichannel significantly suppressed neuronal loss of the spinal cord and extended survival in transgenic mice carrying human superoxide dismutase 1 with G93A or G37R mutation as an amyotrophic lateral sclerosis mouse model. Moreover, blockade of gap junction hemichannel also significantly improved memory impairments without altering amyloid β deposition in double transgenic mice expressing human amyloid precursor protein with K595N and M596L mutations and presenilin 1 with A264E mutation as an Alzheimer's disease mouse model.Our results suggest that gap junction hemichannel blockers may represent a new therapeutic strategy to target neurotoxic microglia specifically and prevent microglia-mediated neuronal death in various neurodegenerative diseases

Delivery of organics to Mars through asteroid and comet impacts

Preliminary results show that the asteroid-borne organic flux on Mars is comparable to the IPD rate; asteroids certainly cannot be neglected. Comets, on the other hand, contribute only 0.01% of the IDP-borne rate and can be neglected in the process of organic delivery to Mars

Delivery of organics to Mars through asteroid and comet impacts

Preliminary results show that the asteroid-borne organic flux on Mars is comparable to the IPD rate; asteroids certainly cannot be neglected. Comets, on the other hand, contribute only 0.01% of the IDP-borne rate and can be neglected in the process of organic delivery to Mars

Cell cycle inhibition provides neuroprotection and reduces glial proliferation and scar formation after traumatic brain injury

Traumatic brain injury (TBI) causes neuronal apoptosis, inflammation, and reactive astrogliosis, which contribute to secondary tissue loss, impaired regeneration, and associated functional disabilities. Here, we show that up-regulation of cell cycle components is associated with caspase-mediated neuronal apoptosis and glial proliferation after TBI in rats. In primary neuronal and astrocyte cultures, cell cycle inhibition (including the cyclin-dependent kinase inhibitors flavopiridol, roscovitine, and olomoucine) reduced up-regulation of cell cycle proteins, limited neuronal cell death after etoposide-induced DNA damage, and attenuated astrocyte proliferation. After TBI in rats, flavopiridol reduced cyclin D1 expression in neurons and glia in ipsilateral cortex and hippocampus. Treatment also decreased neuronal cell death and lesion volume, reduced astroglial scar formation and microglial activation, and improved motor and cognitive recovery. The ability of cell cycle inhibition to decrease both neuronal cell death and reactive gliosis after experimental TBI suggests that this treatment approach may be useful clinically