First observations of sea ice flexural–gravity waves with ground-based radar interferometry in Utqiaġvik, Alaska

We investigate the application of ground-based radar interferometry for measuring flexural–gravity waves in sea ice. We deployed a GAMMA Portable Radar Interferometer (GPRI) on top of a grounded iceberg surrounded by landfast sea ice near Utqiaġvik, Alaska. The GPRI collected 238 acquisitions in stare mode during a period of moderate lateral ice motion during 23–24 April 2021. Individual 30 s interferograms exhibit ∼ 20–50 s periodic motion indicative of propagating infragravity waves with ∼ 1 mm amplitudes. Results include examples of onshore wave propagation at the speed predicted by the water depth and a possible edge wave along an ice discontinuity. Findings are supported through comparison with on-ice Ice Wave Rider (IWR) accelerometers and modeled wave propagation. These results suggest that the GPRI can be a valuable tool to track wave propagation through sea ice and possibly detect changes in such properties across variable ice conditions.</p

Neuroinflammation and structural injury of the fetal ovine brain following intra-amniotic Candida albicans exposure.

BackgroundIntra-amniotic Candida albicans (C. Albicans) infection is associated with preterm birth and high morbidity and mortality rates. Survivors are prone to adverse neurodevelopmental outcomes. The mechanisms leading to these adverse neonatal brain outcomes remain largely unknown. To better understand the mechanisms underlying C. albicans-induced fetal brain injury, we studied immunological responses and structural changes of the fetal brain in a well-established translational ovine model of intra-amniotic C. albicans infection. In addition, we tested whether these potential adverse outcomes of the fetal brain were improved in utero by antifungal treatment with fluconazole.MethodsPregnant ewes received an intra-amniotic injection of 10(7) colony-forming units C. albicans or saline (controls) at 3 or 5 days before preterm delivery at 0.8 of gestation (term ~ 150 days). Fetal intra-amniotic/intra-peritoneal injections of fluconazole or saline (controls) were administered 2 days after C. albicans exposure. Post mortem analyses for fungal burden, peripheral immune activation, neuroinflammation, and white matter/neuronal injury were performed to determine the effects of intra-amniotic C. albicans and fluconazole treatment.ResultsIntra-amniotic exposure to C. albicans caused a severe systemic inflammatory response, illustrated by a robust increase of plasma interleukin-6 concentrations. Cerebrospinal fluid cultures were positive for C. albicans in the majority of the 3-day C. albicans-exposed animals whereas no positive cultures were present in the 5-day C. albicans-exposed and fluconazole-treated animals. Although C. albicans was not detected in the brain parenchyma, a neuroinflammatory response in the hippocampus and white matter was seen which was characterized by increased microglial and astrocyte activation. These neuroinflammatory changes were accompanied by structural white matter injury. Intra-amniotic fluconazole reduced fetal mortality but did not attenuate neuroinflammation and white matter injury.ConclusionsIntra-amniotic C. albicans exposure provoked acute systemic and neuroinflammatory responses with concomitant white matter injury. Fluconazole treatment prevented systemic inflammation without attenuating cerebral inflammation and injury

Nonequilibrium relaxation of the two-dimensional Ising model: Series-expansion and Monte Carlo studies

We study the critical relaxation of the two-dimensional Ising model from a fully ordered configuration by series expansion in time t and by Monte Carlo simulation. Both the magnetization (m) and energy series are obtained up to 12-th order. An accurate estimate from series analysis for the dynamical critical exponent z is difficult but compatible with 2.2. We also use Monte Carlo simulation to determine an effective exponent, z_eff(t) = - {1/8} d ln t /d ln m, directly from a ratio of three-spin correlation to m. Extrapolation to t = infinity leads to an estimate z = 2.169 +/- 0.003.Comment: 9 pages including 2 figure

Iceberg topography and volume classification using TanDEM-X interferometry

Icebergs in polar regions affect water salinity, alter marine habitats, and impose serious hazards on maritime operations and navigation. These impacts mainly depend on the iceberg volume, which remains an elusive parameter to measure. We investigate the capability of TanDEM-X bistatic single-pass synthetic aperture radar interferometry (InSAR) to derive iceberg subaerial morphology and infer total volume. We cross-verify InSAR results with Operation IceBridge (OIB) data acquired near Wordie Bay, Antarctica, as part of the OIB/TanDEM-X Antarctic Science Campaign (OTASC). While icebergs are typically classified according to size based on length or maximum height, we develop a new volumetric classification approach for applications where iceberg volume is relevant. For icebergs with heights exceeding 5 m, we find iceberg volumes derived from TanDEM-X and OIB data match within 7 %. We also derive a range of possible iceberg keel depths relevant to grounding and potential impacts on subsea installations. These results suggest that TanDEM-X could pave the way for future single-pass interferometric systems for scientific and operational iceberg mapping and classification based on iceberg volume and keel depth

Instantaneous sea ice drift speed from TanDEM-X interferometry

The drift of sea ice is an important geophysical process with widespread implications for the ocean energy budget and ecosystems. Drifting sea ice can also threaten marine operations and present a hazard for ocean vessels and installations. Here, we evaluate single-pass along-track synthetic aperture radar (SAR) interferometry (S-ATI) as a tool to assess ice drift while discussing possible applications and inherent limitations. Initial validation shows that TanDEM-X phase-derived drift speed corresponds well with drift products from a ground-based radar at Utqiaġvik, Alaska. Joint analysis of TanDEM-X and Sentinel-1 data covering the Fram Strait demonstrates that S-ATI can help quantify the opening/closing rate of leads with possible applications for navigation. S-ATI enables an instantaneous assessment of ice drift and dynamic processes that are otherwise difficult to observe. For instance, by evaluating sea ice drift through the Vilkitsky Strait, Russia, we identified short-lived transient convergence patterns. We conclude that S-ATI enables the identification and analysis of potentially important dynamic processes (e.g., drift, rafting, and ridging). However, current limitations of S-ATI are significant (e.g., data availability and they presently only provide the cross-track vector component of the ice drift field) but may be significantly reduced with future SAR systems.</p

The Growth and Tumor Suppressors NORE1A and RASSF1A Are Targets for Calpain-Mediated Proteolysis

Background: NORE1A and RASSF1A are growth and tumour suppressors inactivated in a variety of cancers. Methylation of NORE1A and RASSF1A promoters is the predominant mechanism for downregulation of these proteins; however, other mechanisms are likely to exist. Methodology/Principal Findings: Here we describe a proteolysis of NORE1A and RASSF1A by calpains as alternative mechanism of their downregulation. Extracts of H358 cell line, a human bronchoalveolar carcinoma, and H460, a large cell carcinoma, were capable of proteolysis of NORE1A protein in the calpain-dependent manner. Likewise, RASSF1A tumor suppressor was proteolyzed by the H358 cell extract. Addition of calpain inhibitor to H358 and H460 cells growing in tissue culture resulted in re-expression of endogenous NORE1A. A survey of 10 human lung tumours revealed that three of them contain an activity capable of inducing NORE1A degradation. Conclusions/Significance: Thus, degradation by calpains is a novel mechanism for downregulation of NORE1A and RASSF1A proteins and might be the mechanism allowing cancer cells to escape growth suppression

Enhanced antitumoral activity of TLR7 agonists via activation of human endogenous retroviruses by HDAC inhibitors

In this work, we are reporting that “Shock and Kill”, a therapeutic approach designed to eliminate latent HIV from cell reservoirs, is extrapolatable to cancer therapy. This is based on the observation that malignant cells express a spectrum of human endogenous retroviral elements (HERVs) which can be transcriptionally boosted by HDAC inhibitors. The endoretroviral gene HERV-V2 codes for an envelope protein, which resembles syncytins. It is significantly overexpressed upon exposure to HDAC inhibitors and can be effectively targeted by simultaneous application of TLR7/8 agonists, triggering intrinsic apoptosis. We demonstrated that this synergistic cytotoxic effect was accompanied by the functional disruption of the TLR7/8-NFκB, Akt/PKB, and Ras-MEK-ERK signalling pathways. CRISPR/Cas9 ablation of TLR7 and HERV-V1/V2 curtailed apoptosis significantly, proving the pivotal role of these elements in driving cell death. The effectiveness of this new approach was confirmed in ovarian tumour xenograft studies, revealing a promising avenue for future cancer therapies

Ras-association domain family 1C protein promotes breast cancer cell migration and attenuates apoptosis

<p>Abstract</p> <p>Background</p> <p>The Ras association domain family 1 (RASSF1) gene is a Ras effector encoding two major mRNA forms, RASSF1A and RASSF1C, derived by alternative promoter selection and alternative mRNA splicing. RASSF1A is a tumor suppressor gene. However, very little is known about the function of RASSF1C both in normal and transformed cells.</p> <p>Methods</p> <p>Gene silencing and over-expression techniques were used to modulate RASSF1C expression in human breast cancer cells. Affymetrix-microarray analysis was performed using T47D cells over-expressing RASSF1C to identify RASSF1C target genes. RT-PCR and western blot techniques were used to validate target gene expression. Cell invasion and apoptosis assays were also performed.</p> <p>Results</p> <p>In this article, we report the effects of altering RASSF1C expression in human breast cancer cells. We found that silencing RASSF1C mRNA in breast cancer cell lines (MDA-MB231 and T47D) caused a small but significant decrease in cell proliferation. Conversely, inducible over-expression of RASSF1C in breast cancer cells (MDA-MB231 and T47D) resulted in a small increase in cell proliferation. We also report on the identification of novel RASSF1C target genes. RASSF1C down-regulates several pro-apoptotic and tumor suppressor genes and up-regulates several growth promoting genes in breast cancer cells. We further show that down-regulation of caspase 3 via overexpression of RASSF1C reduces breast cancer cells' sensitivity to the apoptosis inducing agent, etoposide. Furthermore, we found that RASSF1C over-expression enhances T47D cell invasion/migration <it>in vitro</it>.</p> <p>Conclusion</p> <p>Together, our findings suggest that RASSF1C, unlike RASSF1A, is not a tumor suppressor, but instead may play a role in stimulating metastasis and survival in breast cancer cells.</p