17 research outputs found
Stability of Terrestrial Planets in the Habitable Zone of Gl 777 A, HD 72659, Gl 614, 47 Uma and HD 4208
We have undertaken a thorough dynamical investigation of five extrasolar
planetary systems using extensive numerical experiments. The systems Gl 777 A,
HD 72659, Gl 614, 47 Uma and HD 4208 were examined concerning the question of
whether they could host terrestrial like planets in their habitable zones
(=HZ). First we investigated the mean motion resonances between fictitious
terrestrial planets and the existing gas giants in these five extrasolar
systems. Then a fine grid of initial conditions for a potential terrestrial
planet within the HZ was chosen for each system, from which the stability of
orbits was then assessed by direct integrations over a time interval of 1
million years. The computations were carried out using a Lie-series integration
method with an adaptive step size control. This integration method achieves
machine precision accuracy in a highly efficient and robust way, requiring no
special adjustments when the orbits have large eccentricities. The stability of
orbits was examined with a determination of the Renyi entropy, estimated from
recurrence plots, and with a more straight forward method based on the maximum
eccentricity achieved by the planet over the 1 million year integration.
Additionally, the eccentricity is an indication of the habitability of a
terrestrial planet in the HZ; any value of e>0.2 produces a significant
temperature difference on a planet's surface between apoapse and periapse. The
results for possible stable orbits for terrestrial planets in habitable zones
for the five systems are summarized as follows: for Gl 777 A nearly the entire
HZ is stable, for 47 Uma, HD 72659 and HD 4208 terrestrial planets can survive
for a sufficiently long time, while for Gl 614 our results exclude terrestrial
planets moving in stable orbits within the HZ.Comment: 14 pages, 18 figures submitted to A&
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Pannexin-1 Channels as Mediators of Neuroinflammation
Neuroinflammation is a major component of central nervous system (CNS) injuries and neurological diseases, including Alzheimer's disease, multiple sclerosis, neuropathic pain, and brain trauma. The activation of innate immune cells at the damage site causes the release of pro-inflammatory cytokines and chemokines, which alter the functionality of nearby tissues and might mediate the recruitment of leukocytes to the injury site. If this process persists or is exacerbated, it prevents the adequate resolution of the inflammation, and ultimately enhances secondary damage. Adenosine 5' triphosphate (ATP) is among the molecules released that trigger an inflammatory response, and it serves as a chemotactic and endogenous danger signal. Extracellular ATP activates multiple purinergic receptors (P2X and P2Y) that have been shown to promote neuroinflammation in a variety of CNS diseases. Recent studies have shown that Pannexin-1 (Panx1) channels are the principal conduits of ATP release from dying cells and innate immune cells in the brain. Herein, we review the emerging evidence that directly implicates Panx-1 channels in the neuroinflammatory response in the CNS
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Myeloid Pannexin-1 mediates acute leukocyte infiltration and leads to worse outcomes after brain trauma
BackgroundNeuroinflammation is a major component of secondary damage after traumatic brain injury (TBI). We recently reported that pharmacological inhibition of Pannexin-1 (Panx1) channels markedly reduced the inflammatory response after TBI. Panx1 channels have been shown to be important conduits for adenosine 5'-triphosphate (ATP) release and are associated with leukocyte infiltration and pyroptosis. Because Panx1 blockers significantly decrease ATP release and migration of activated microglia and other myeloid cells (such as monocyte-derived macrophages and dendritic cells) in vitro, we hypothesized that myeloid Panx1 channels play a specific role in immune cell infiltration promoting tissue damage following TBI.MethodsThe murine-controlled cortical impact (CCI) model was used on myeloid-specific Panx1 conditional knockout (Cx3cr1-Cre::Panx1fl/fl) mice to determine whether myeloid Panx1 mediates neuroinflammation and brain damage. Immune cell infiltration was measured using flow cytometry. Locomotor and memory functions were measured using the rotarod and Barnes maze test, respectively. The levels of biomarkers for tissue damage and blood-brain barrier leakage were measured using western blot and magnetic resonance imaging. Panx1 channel activity was measured with ex vivo dye uptake assays, using flow cytometry and confocal microscopy.ResultsCCI-injured Cx3cr1-Cre::Panx1fl/fl mice showed markedly reduced immune cell infiltration to the brain parenchyma compared with Panx1fl/fl mice. As expected, Panx1 dependent activity, assessed by dye uptake, was markedly reduced only in myeloid cells from Cx3cr1-Cre::Panx1fl/fl mice. The expression of biomarkers of tissue damage was significantly reduced in the CCI-injured Cx3cr1-Cre::Panx1fl/fl mice compared with Panx1fl/fl mice. In line with this, magnetic resonance imaging showed reduced blood-brain barrier leakage in CCI-injured Cx3cr1-Cre::Panx1fl/fl mice. There was also a significant improvement in motor and memory function in Cx3cr1-Cre::Panx1fl/fl mice when compared with Panx1fl/fl mice within a week post-CCI injury.ConclusionOur data demonstrate that CCI-related outcomes correlate with Panx1 channel function in myeloid cells, indicating that activation of Panx1 channels in myeloid cells is a major contributor to acute brain inflammation following TBI. Importantly, our data indicate myeloid Panx1 channels could serve as an effective therapeutic target to improve outcome after TBI