Permafrost

Permafrost is perennially frozen ground, such as soil, rock, and ice. In permafrost regions, plant and microbial life persists primarily in the near-surface soil that thaws every summer, called the ‘active layer’ (Figure 20). The cold and wet conditions in many permafrost regions limit decomposition of organic matter. In combination with soil mixing processes caused by repeated freezing and thawing, this has led to the accumulation of large stocks of soil organic carbon in the permafrost zone over multi-millennial timescales. As the climate warms, permafrost carbon could be highly vulnerable to climatic warming. Permafrost occurs primarily in high latitudes (e.g. Arctic and Antarctic) and at high elevation (e.g. Tibetan Plateau, Figure 21). The thickness of permafrost varies from less than 1 m (in boreal peatlands) to more than 1 500 m (in Yakutia). The coldest permafrost is found in the Transantarctic Mountains in Antarctica (−36°C) and in northern Canada for the Northern Hemisphere (-15°C; Obu et al., 2019, 2020). In contrast, some of the warmest permafrost occurs in peatlands in areas with mean air temperatures above 0°C. Here permafrost exists because thick peat layers insulate the ground during the summer. Most of the permafrost existing today formed during cold glacials (e.g. before 12 000 years ago) and has persisted through warmer interglacials. Some shallow permafrost (max 30–70m depth) formed during the Holocene (past 5000 years) and some even during the Little Ice Age from 400–150 years ago. There are few extensive regions suitable for row crop agriculture in the permafrost zone. Additionally, in areas where large-scale agriculture has been conducted, ground destabilization has been common. Surface disturbance such as plowing or trampling of vegetation can alter the thermal regime of the soil, potentially triggering surface subsidence or abrupt collapse. This may influence soil hydrology, nutrient cycling, and organic matter storage. These changes often have acute and negative consequences for continued agricultural use of such landscapes. Thus, row-crop agriculture could have a negative impact on permafrost (e.g. Grünzweig et al., 2014). Conversely, animal husbandry is widespread in the permafrost zone, including horses, cattle, and reindeer

Permafrost and Climate Change: Carbon Cycle Feedbacks From the Warming Arctic

Rapid Arctic environmental change affects the entire Earth system as thawing permafrost ecosystems release greenhouse gases to the atmosphere. Understanding how much permafrost carbon will be released, over what time frame, and what the relative emissions of carbon dioxide and methane will be is key for understanding the impact on global climate. In addition, the response of vegetation in a warming climate has the potential to offset at least some of the accelerating feedback to the climate from permafrost carbon. Temperature, organic carbon, and ground ice are key regulators for determining the impact of permafrost ecosystems on the global carbon cycle. Together, these encompass services of permafrost relevant to global society as well as to the people living in the region and help to determine the landscape-level response of this region to a changing climate

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Crystallinity Effects in Sequentially Processed and Blend-Cast Bulk-Heterojunction Polymer/Fullerene Photovoltaics

Although most polymer/fullerene-based solar cells are cast from a blend of the components in solution, it is also possible to sequentially process the polymer and fullerene layers from quasi-orthogonal solvents. Sequential processing (SqP) not only produces photovoltaic devices with efficiencies comparable to the more traditional bulk heterojunction (BHJ) solar cells produced by blend casting (BC) but also offers the advantage that the polymer and fullerene layers can be optimized separately. In this paper, we explore the morphology produced when sequentially processing polymer/fullerene solar cells and compare it to the BC morphology. We find that increasing polymer regioregularity leads to the opposite effect in SqP and BC BHJ solar cells. We start by constructing a series of SqP and BC solar cells using different types of poly(3-hexylthiophene) (P3HT) that vary in regioregulary and polydispersity combined with [6,6]-phenyl-C61-butyric-acid-methyl-ester (PCBM). We use grazing incidence wide-angle X-ray scattering to demonstrate how strongly changes in the P3HT and PCBM crystallinity upon thermal annealing of SqP and BC BHJ films depend on polymer regioregularity. For SqP devices, low regioregularity P3HT films that possess more amorphous regions allow for more PCBM crystallite growth and thus show better photovoltaic device efficiency. On the other hand, highly regioregular P3HT leads to a more favorable morphology and better device efficiency for BC BHJ films. Comparing the photovoltaic performance and structural characterization indicates that the mechanisms controlling morphology in the active layers are fundamentally different for BHJs formed via SqP and BC. Most importantly, we find that nanoscale morphology in both SqP and BC BHJs can be systematically controlled by tuning the amorphous fraction of polymer in the active layer. © 2014 American Chemical Society

Influence of an immunodominant herpes simplex virus type 1 CD8+ T cell epitope on the target hierarchy and function of subdominant CD8+ T cells.

Herpes simplex virus type 1 (HSV-1) latency in sensory ganglia such as trigeminal ganglia (TG) is associated with a persistent immune infiltrate that includes effector memory CD8+ T cells that can influence HSV-1 reactivation. In C57BL/6 mice, HSV-1 induces a highly skewed CD8+ T cell repertoire, in which half of CD8+ T cells (gB-CD8s) recognize a single epitope on glycoprotein B (gB498-505), while the remainder (non-gB-CD8s) recognize, in varying proportions, 19 subdominant epitopes on 12 viral proteins. The gB-CD8s remain functional in TG throughout latency, while non-gB-CD8s exhibit varying degrees of functional compromise. To understand how dominance hierarchies relate to CD8+ T cell function during latency, we characterized the TG-associated CD8+ T cells following corneal infection with a recombinant HSV-1 lacking the immunodominant gB498-505 epitope (S1L). S1L induced a numerically equivalent CD8+ T cell infiltrate in the TG that was HSV-specific, but lacked specificity for gB498-505. Instead, there was a general increase of non-gB-CD8s with specific subdominant epitopes arising to codominance. In a latent S1L infection, non-gB-CD8s in the TG showed a hierarchy targeting different epitopes at latency compared to at acute times, and these cells retained an increased functionality at latency. In a latent S1L infection, these non-gB-CD8s also display an equivalent ability to block HSV reactivation in ex vivo ganglionic cultures compared to TG infected with wild type HSV-1. These data indicate that loss of the immunodominant gB498-505 epitope alters the dominance hierarchy and reduces functional compromise of CD8+ T cells specific for subdominant HSV-1 epitopes during viral latency

Stimulation of acute TG-resident CD8⁺ T cell populations with WT, SIL, or L8A gB peptides.

<p>B6 mice received corneal infections with HSV-1 expressing WT, S1L, or L8A gB. TG were obtained at 8 dpi, dispersed into single cell suspensions, and the endogenous CD8⁺ T cells were stimulated for 6 hours with B6WT3 fibroblasts pulsed individually with WT, S1L, or L8A gB_498-505 peptides, in the presence of brefeldin A. Cells were surface stained for CD45 and CD8, followed by an intracellular stain for IFNγ. The data are represented as the mean percentage of CD8⁺ T cells that produced IFNγ +/- SEM (n = 5 mice per group). * represents significance of p<0.0001 for each group compared to gB peptide stimulation of wild-type infected control (first column) using one-way ANOVA with Dunnett’s multiple comparisons posttest.</p

Primer sequences (complementary to the coding sequence) used in PCR to generate mutations in the gB epitope (SSIEFARL) region.

<p>Primer sequences (complementary to the coding sequence) used in PCR to generate mutations in the gB epitope (SSIEFARL) region.</p

Acute CD8⁺ T cell infiltrates in the ganglia of mice after corneal infection with WT HSV-1 or recombinant HSV-1 containing gB_498-505 mutations.

<p>Corneas of mice were infected with 1x10⁵ PFU/eye of HSV-1 WT, S1L, or L8A. At 8 dpi (peak CD8⁺ T cell infiltrate), the TG, spleen, or DLN were dissociated into single cell suspensions and surface stained with antibodies to CD45, CD3, CD8 and with MHC-I gB_498-505 tetramer as detailed in Methods. Cells were analyzed by flow cytometry, and the data are presented as the mean +/- SEM (n = 5 mice, 10 TGs) of <b>(A)</b> absolute number of CD3⁺CD8⁺ T cells per TG, <b>(B)</b> the percent of gB_498-505 tetramer positive CD8⁺ T cells in each TG, or <b>(C, D)</b> the total number of gB_498-505 tetramer specific cells per spleen and local DLN. The experiment shown is representative of three additional experiments, all producing similar results. The absolute numbers of CD8⁺ T cells induced in the TG with each virus were not statistically different as shown by a one-way ANOVA followed by Tukey’s posttest (p = 0.58).</p

Certain subdominant HSV-1 epitopes become more functional and arise to codominance in TG during HSV-1 S1L latency.

<p>Studies were as detailed in <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1006732#ppat.1006732.g009" target="_blank">Fig 9</a>, except that TGs were harvested from infected mice at 30–33 dpi. <b>(A)</b> The order of epitopes is identical to those shown in <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1006732#ppat.1006732.g009" target="_blank">Fig 9</a>. For clarity, only the non-gB_498-505 responses are shown in A, but the total percentages are displayed in (B). The bars represent the total number of CD8⁺ T cells producing IFNγ⁺ in response to peptide stimulation, and error bars represent SEM. For significantly different populations, the average fold change increase in population over wild-type is shown. <b>(B)</b> Total fraction of gB_498-505 or non-gB-CD8s depicted in figure (A) that are responding to peptide stimulations. <b>(C)</b> Total fraction of the non-gB_498-505 specific CD8+ T cells depicted in figure (A) that make IFNγ after peptide stimulation. <b>(D)</b> 30 dpi TGs suspensions were stained with tetramers specific to RR1-specific subdominant CD8+ T cell populations (tetramers for RR1 982–989 and 822–829). Shown are the total number of each RR1-specific CD8+ T cell population per TG. The total number of single functional (IFNγ⁺) or multifunctional (IFNγ⁺TNFα⁺CD107a⁺) CD8⁺ T cells after stimulation with a combination RR1 982–989 and 822–829 peptides is also shown. N = 3–7 TG equivalents per group. A t-test was performed for each matched pair of responding CD8⁺ T cells, and a * denotes p<0.05.</p

Growth of HSV gB mutants <i>in vitro</i> and <i>in vivo</i>.

<p><b>(A)</b> Virus growth in the TG of B6 mice was determined at 4 days post ocular infection with 1x10⁵ PFU of either HSV-1 WT or HSV-1 containing the gB_498-505 epitope mutants detailed in <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1006732#ppat.1006732.t001" target="_blank">Table 1</a>. TG were harvested and subjected to three freeze thaw cycles and infectious virus released into the supernatant was titrated on Vero cells. The graph represents the mean virus titer for each virus ± SEM of the mean (n = 5 mice). This is a representative of two separate studies with similar results. <b>(B)</b> Genome copy number determined by qPCR in the TG of mice infected with HSV-1 WT, S1L, or L8A following harvest at day 8 post ocular infection (n = 10). Values are representative of the total copies per TG. <b>(C,D)</b> Monolayer cultures of Vero cells were infected at a multiplicity of infection (MOI) of 10 PFU/cell (high MOI Growth Curve) or 0.01 PFU/cell (Low MOI Growth Curve) respectively with HSV-1 WT, S1L, or L8A. At the indicated hours post-infection, cells and supernatants were pooled, subjected to three freeze–thaw cycles and the viral titers were determined by plaque assay. The mean PFU/culture ± standard error of the means (SEM) is shown at each time.</p