Towards critical white ice conditions in lakes under global warming.

The quality of lake ice is of uppermost importance for ice safety and under-ice ecology, but its temporal and spatial variability is largely unknown. Here we conducted a coordinated lake ice quality sampling campaign across the Northern Hemisphere during one of the warmest winters since 1880 and show that lake ice during 2020/2021 commonly consisted of unstable white ice, at times contributing up to 100% to the total ice thickness. We observed that white ice increased over the winter season, becoming thickest and constituting the largest proportion of the ice layer towards the end of the ice cover season when fatal winter drownings occur most often and light limits the growth and reproduction of primary producers. We attribute the dominance of white ice before ice-off to air temperatures varying around the freezing point, a condition which occurs more frequently during warmer winters. Thus, under continued global warming, the prevalence of white ice is likely to substantially increase during the critical period before ice-off, for which we adjusted commonly used equations for human ice safety and light transmittance through ice.

Erythropoietin improved cognitive function and decreased hippocampal caspase activity in rat pups after traumatic brain injury.

UNLABELLED: Traumatic brain injury (TBI) is a leading cause of acquired neurologic disability in children. Erythropoietin (EPO), an anti-apoptotic cytokine, improved cognitive outcome in adult rats after TBI. To our knowledge, EPO has not been studied in a developmental TBI model. HYPOTHESIS: We hypothesized that EPO would improve cognitive outcome and increase neuron fraction in the hippocampus in 17-day-old (P17) rat pups after controlled cortical impact (CCI). METHODS: EPO or vehicle was given at 1, 24, and 48 h after CCI and at post injury day (PID) 7. Cognitive outcome at PID14 was assessed using Novel Object Recognition (NOR). Hippocampal EPO levels, caspase activity, and mRNA levels of the apoptosis factors Bcl2, Bax, Bcl-xL, and Bad were measured during the first 14 days after injury. Neuron fraction and caspase activation in CA1, CA3, and DG were studied at PID2. RESULTS: EPO normalized recognition memory after CCI. EPO blunted the increased hippocampal caspase activity induced by CCI at PID1, but not at PID2. EPO increased neuron fraction in CA3 at PID2. Brain levels of exogenous EPO appeared low relative to endogenous. Timing of EPO administration was associated with temporal changes in hippocampal mRNA levels of EPO and pro-apoptotic factors. Conclusion/Speculation: EPO improved recognition memory, increased regional hippocampal neuron fraction, and decreased caspase activity in P17 rats after CCI. We speculate that EPO improved cognitive outcome in rat pups after CCI as a result of improved neuronal survival via inhibition of caspase-dependent apoptosis early after injury.

Anisotropic interfacial tension, contact angles, and line tensions: a graphics-processing-unit-based Monte Carlo study of the Ising model.

As a generic example for crystals where the crystal-fluid interface tension depends on the orientation of the interface relative to the crystal lattice axes, the nearest-neighbor Ising model on the simple cubic lattice is studied over a wide temperature range, both above and below the roughening transition temperature. Using a thin-film geometry L(x)×L(y)×L(z) with periodic boundary conditions along the z axis and two free L(x)×L(y) surfaces at which opposing surface fields ±H(1) act, under conditions of partial wetting, a single planar interface inclined under a contact angle θ<π/2 relative to the yz plane is stabilized. In the y direction, a generalization of the antiperiodic boundary condition is used that maintains the translational invariance in the y direction despite the inhomogeneity of the magnetization distribution in this system. This geometry allows a simultaneous study of the angle-dependent interface tension, the contact angle, and the line tension (which depends on the contact angle, and on temperature). All these quantities are extracted from suitable thermodynamic integration procedures. In order to keep finite-size effects as well as statistical errors small enough, rather large lattice sizes (of the order of 46 million sites) were found to be necessary, and the availability of very efficient code implementation of graphics processing units was crucial for the feasibility of this study.

Developmental traumatic brain injury decreased brain derived neurotrophic factor expression late after injury.

Pediatric traumatic brain injury (TBI) is a major cause of acquired cognitive dysfunction in children. Hippocampal Brain Derived Neurotrophic Factor (BDNF) is important for normal cognition. Little is known about the effects of TBI on BDNF levels in the developing hippocampus. We used controlled cortical impact (CCI) in the 17 day old rat pup to test the hypothesis that CCI would first increase rat hippocampal BDNF mRNA/protein levels relative to SHAM and Naïve rats by post injury day (PID) 2 and then decrease BDNF mRNA/protein by PID14. Relative to SHAM, CCI did not change BDNF mRNA/protein levels in the injured hippocampus in the first 2 days after injury but did decrease BDNF protein at PID14. Surprisingly, BDNF mRNA decreased at PID 1, 3, 7 and 14, and BDNF protein decreased at PID 2, in SHAM and CCI hippocampi relative to Naïve. In conclusion, TBI decreased BDNF protein in the injured rat pup hippocampus 14 days after injury. BDNF mRNA levels decreased in both CCI and SHAM hippocampi relative to Naïve, suggesting that certain aspects of the experimental paradigm (such as craniotomy, anesthesia, and/or maternal separation) may decrease the expression of BDNF in the developing hippocampus. While BDNF is important for normal cognition, no inferences can be made regarding the cognitive impact of any of these factors. Such findings, however, suggest that meticulous attention to the experimental paradigm, and possible inclusion of a Naïve group, is warranted in studies of BDNF expression in the developing brain after TBI.

Traumatic brain injury increased IGF-1B mRNA and altered IGF-1 exon 5 and promoter region epigenetic characteristics in the rat pup hippocampus.

Traumatic brain injury (TBI) is a major cause of acquired cognitive disability in childhood. Such disability may be blunted by enhancing the brain's endogenous neuroprotective response. An important endogenous neuroprotective response is the insulin-like growth factor-1 (IGF-1) mRNA variant, IGF-1B. IGF-1B mRNA, characterized by exon 5 inclusion, encodes the IGF-1 and Eb peptides. IGF-1A mRNA excludes exon 5 and encodes the IGF-1 and Ea peptides. A region in the human IGF-1B homologue acts as an exon-splicing enhancer (ESE) to increase IGF-1B mRNA. It is not known if TBI is associated with increased brain IGF-1B mRNA. Epigenetic modifications may underlie altered gene expression in the brain after TBI. We hypothesized that TBI would increase hippocampal IGF-1B mRNA in 17-day-old rats, associated with DNA methylation and/or histone modifications at the promoter site 1 (P1) or exon 5/ESE region. Hippocampi from rat pups after controlled cortical impact (CCI) were used to measure IGF-1B mRNA, DNA methylation, and histone modifications at the P1, P2, and exon5/ESE regions. In CCI hippocampi, IGF-1B mRNA peaked at post-injury day (PID) 2 (1700±320% sham), but normalized by PID 14. IGF-1A peaked at PID 3 (280±52% sham), and remained elevated at PID 14. Increased IGF-1B mRNA was associated with increased methylation at P1, and increased histone modifications associated with gene activation at P2 and exon5/ESE, together with differential methylation in the exon 5/ESE regions. We report for the first time that hippocampal IGF-1B mRNA increased after developmental TBI. We speculate that epigenetic modifications at the P2 and exon 5/ESE regions are important in the regulation of IGF-1B mRNA expression. The exon 5/ESE region may present a means for future therapies to target IGF-1B transcription after TBI.

Curvature dependence of surface free energy of liquid drops and bubbles: A simulation study.

We study the excess free energy due to phase coexistence of fluids by Monte Carlo simulations using successive umbrella sampling in finite L×L×L boxes with periodic boundary conditions. Both the vapor-liquid phase coexistence of a simple Lennard-Jones fluid and the coexistence between A-rich and B-rich phases of a symmetric binary (AB) Lennard-Jones mixture are studied, varying the density ρ in the simple fluid or the relative concentration x(A) of A in the binary mixture, respectively. The character of phase coexistence changes from a spherical droplet (or bubble) of the minority phase (near the coexistence curve) to a cylindrical droplet (or bubble) and finally (in the center of the miscibility gap) to a slablike configuration of two parallel flat interfaces. Extending the analysis of Schrader et al., [Phys. Rev. E 79, 061104 (2009)], we extract the surface free energy γ(R) of both spherical and cylindrical droplets and bubbles in the vapor-liquid case and present evidence that for R→∞ the leading order (Tolman) correction for droplets has sign opposite to the case of bubbles, consistent with the Tolman length being independent on the sign of curvature. For the symmetric binary mixture, the expected nonexistence of the Tolman length is confirmed. In all cases and for a range of radii R relevant for nucleation theory, γ(R) deviates strongly from γ(∞) which can be accounted for by a term of order γ(∞)/γ(R)-1∝R(-2). Our results for the simple Lennard-Jones fluid are also compared to results from density functional theory, and we find qualitative agreement in the behavior of γ(R) as well as in the sign and magnitude of the Tolman length.

Early and sustained increase in the expression of hippocampal IGF-1, but not EPO, in a developmental rodent model of traumatic brain injury.

Pediatric traumatic brain injury (pTBI) is the leading cause of traumatic death and disability in children in the United States. Impaired learning and memory in these young survivors imposes a heavy toll on society. In adult TBI (aTBI) models, cognitive outcome improved after administration of erythropoietin (EPO) or insulin-like growth factor-1 (IGF-1). Little is known about the production of these agents in the hippocampus, a brain region critical for learning and memory, after pTBI. Our objective was to describe hippocampal expression of EPO and IGF-1, together with their receptors (EPOR and IGF-1R, respectively), over time after pTBI in 17-day-old rats. We used the controlled cortical impact (CCI) model and measured hippocampal mRNA levels of EPO, IGF-1, EPOR, IGF-1R, and markers of caspase-dependent apoptosis (bcl2, bax, and p53) at post-injury days (PID) 1, 2, 3, 7, and 14. CCI rats performed poorly on Morris water maze testing of spatial working memory, a hippocampally-based cognitive function. Apoptotic markers were present early and persisted for the duration of the study. EPO in our pTBI model increased much later (PID7) than in aTBI models (12 h), while EPOR and IGF-1 increased at PID1 and PID2, respectively, similar to data from aTBI models. Our data indicate that EPO expression showed a delayed upregulation post-pTBI, while EPOR increased early. We speculate that administration of EPO in the first 1-2 days after pTBI would increase hippocampal neuronal survival and function.