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A large new grater exposes the limits of water ice on Mars
Water ice in the Martian mid-latitudes has advanced and retreated in response to variations in the planet's orbit, obliquity, and climate. A 150 m-diameter new impact crater near 35°N provides the lowest-latitude impact exposure of subsurface ice on Mars. This is the largest known ice-exposing crater and provides key constraints on Martian climate history. This crater indicates a regional, relatively pure ice deposit that is unstable and has nearly vanished. In the past, this deposit may have been tens of meters thick and extended equatorward of 35°N. We infer that it is overlain by pore ice emplaced during temporary stable intervals, due to recent climate variability. The marginal survival of ice here suggests that it is near the edge of shallow ice that regularly exchanges with the atmosphere
Taking the pulse of Mars via dating of a plume-fed volcano
Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. The attached file is the published version of the article
Spiral ligament fibrocyte-derived MCP-1/CCL2 contributes to inner ear inflammation secondary to nontypeable H. influenzae-induced otitis media
<p>Abstract</p> <p>Background</p> <p>Otitis media (OM), one of the most common pediatric infectious diseases, causes inner ear inflammation resulting in vertigo and sensorineural hearing loss. Previously, we showed that spiral ligament fibrocytes (SLFs) recognize OM pathogens and up-regulate chemokines. Here, we aim to determine a key molecule derived from SLFs, contributing to OM-induced inner ear inflammation.</p> <p>Methods</p> <p>Live NTHI was injected into the murine middle ear through the tympanic membrane, and histological analysis was performed after harvesting the temporal bones. Migration assays were conducted using the conditioned medium of NTHI-exposed SLFs with and without inhibition of MCP-1/CCL2 and CCR2. qRT-PCR analysis was performed to demonstrate a compensatory up-regulation of alternative genes induced by the targeting of MCP-1/CCL2 or CCR2.</p> <p>Results</p> <p>Transtympanic inoculation of live NTHI developed serous and purulent labyrinthitis after clearance of OM. THP-1 cells actively migrated and invaded the extracellular matrix in response to the conditioned medium of NTHI-exposed SLFs. This migratory activity was markedly inhibited by the viral CC chemokine inhibitor and the deficiency of MCP-1/CCL2, indicating that MCP-1/CCL2 is a main attractant of THP-1 cells among the SLF-derived molecules. We further demonstrated that CCR2 deficiency inhibits migration of monocyte-like cells in response to NTHI-induced SLF-derived molecules. Immunolabeling showed an increase in MCP-1/CCL2 expression in the cochlear lateral wall of the NTHI-inoculated group. Contrary to the <it>in vitro </it>data, deficiency of MCP-1/CCL2 or CCR2 did not inhibit OM-induced inner ear inflammation <it>in vivo</it>. We demonstrated that targeting MCP-1/CCL2 enhances NTHI-induced up-regulation of MCP-2/CCL8 in SLFs and up-regulates the basal expression of CCR2 in the splenocytes. We also found that targeting CCR2 enhances NTHI-induced up-regulation of MCP-1/CCL2 in SLFs.</p> <p>Conclusions</p> <p>Taken together, we suggest that NTHI-induced SLF-derived MCP-1/CCL2 is a key molecule contributing to inner ear inflammation through CCR2-mediated recruitment of monocytes. However, deficiency of MCP-1/CCL2 or CCR2 alone was limited to inhibit OM-induced inner ear inflammation due to compensation of alternative genes.</p
Dependence of secondary crater characteristics on downrange distance: high-resolution morphometry and simulations
On average, secondary impact craters are expected to deepen and become more symmetric as impact velocity (vi) increases with downrange distance (L). We have used high-resolution topography (1–2 m/pixel) to characterize the morphometry of secondary craters as a function of L for several well-preserved primary craters on Mars. The secondaries in this study (N = 2644) span a range of diameters (25 m ≤D≤400 m) and estimated impact velocities (0.4 km/s ≤vi≤2 km/s). The range of diameter-normalized rim-to-floor depth (d/D) broadens and reaches a ceiling of d/D≈0.22 at L≈280 km (vi= 1–1.2 km/s), whereas average rim height shows little dependence on vi for the largest craters (h/D≈0.02, D > 60 m). Populations of secondaries that express the following morphometric asymmetries are confined to regions of differing radial extent: planform elongations (L< 110–160 km), taller downrange rims (L < 280 km), and cavities that are deeper uprange (L< 450–500 km). Populations of secondaries with lopsided ejecta were found to extend to at least L ∼ 700 km. Impact hydrocode simulations with iSALE-2D for strong, intact projectile and target materials predict a ceiling for d/D versus L whose trend is consistent with our measurements. This study illuminates the morphometric transition from subsonic to hypervelocity cratering and describes the initial state of secondary crater populations. This has applications to understanding the chronology of planetary surfaces and the long-term evolution of small crater populations