Thermoregulatory traits combine with range shifts to alter the future of montane ant assemblages.

Predicting and understanding the biological response to future climate change is a pressing challenge for humanity. In the 21st century, many species will move into higher latitudes and higher elevations as the climate warms. In addition, the relative abundances of species within local assemblages is likely to change. Both effects have implications for how ecosystems function. Few biodiversity forecasts, however, take account of both shifting ranges and changing abundances. We provide a novel analysis predicting the potential changes to assemblage level relative abundances in the 21st century. We use an established relationship linking ant abundance and their colour and size traits to temperature and UV-B to predict future abundance changes. We also predict future temperature driven range shifts and use these to alter the available species pool for our trait-mediated abundance predictions. We do this across three continents under a low greenhouse gas emissions scenario (RCP2.6) and a business-as-usual scenario (RCP8.5). Under RCP2.6, predicted changes to ant assemblages by 2100 are moderate. On average, species richness will increase by 26%, while species composition and relative abundance structure will be 26% and 30% different, respectively, compared with modern assemblages. Under RCP8.5, however, highland assemblages face almost a tripling of species richness and compositional and relative abundance changes of 66% and 77%. Critically, we predict that future assemblages could be reorganised in terms of which species are common and which are rare: future highland assemblages will not simply comprise upslope shifts of modern lowland assemblages. These forecasts reveal the potential for radical change to montane ant assemblages by the end of the 21st century if temperature increases continue. Our results highlight the importance of incorporating trait-environment relationships into future biodiversity predictions. Looking forward, the major challenge is to understand how ecosystem processes will respond to compositional and relative abundance changes. This article is protected by copyright. All rights reserved

Thermoregulatory traits combine with range shifts to alter the future of montane ant assemblages.

Predicting and understanding the biological response to future climate change is a pressing challenge for humanity. In the 21st century, many species will move into higher latitudes and higher elevations as the climate warms. In addition, the relative abundances of species within local assemblages is likely to change. Both effects have implications for how ecosystems function. Few biodiversity forecasts, however, take account of both shifting ranges and changing abundances. We provide a novel analysis predicting the potential changes to assemblage level relative abundances in the 21st century. We use an established relationship linking ant abundance and their colour and size traits to temperature and UV-B to predict future abundance changes. We also predict future temperature driven range shifts and use these to alter the available species pool for our trait-mediated abundance predictions. We do this across three continents under a low greenhouse gas emissions scenario (RCP2.6) and a business-as-usual scenario (RCP8.5). Under RCP2.6, predicted changes to ant assemblages by 2100 are moderate. On average, species richness will increase by 26%, while species composition and relative abundance structure will be 26% and 30% different, respectively, compared with modern assemblages. Under RCP8.5, however, highland assemblages face almost a tripling of species richness and compositional and relative abundance changes of 66% and 77%. Critically, we predict that future assemblages could be reorganised in terms of which species are common and which are rare: future highland assemblages will not simply comprise upslope shifts of modern lowland assemblages. These forecasts reveal the potential for radical change to montane ant assemblages by the end of the 21st century if temperature increases continue. Our results highlight the importance of incorporating trait-environment relationships into future biodiversity predictions. Looking forward, the major challenge is to understand how ecosystem processes will respond to compositional and relative abundance changes. This article is protected by copyright. All rights reserved

Dioxin Induces Genomic Instability in Mouse Embryonic Fibroblasts

Ionizing radiation and certain other exposures have been shown to induce genomic instability (GI), i.e., delayed genetic damage observed many cell generations later in the progeny of the exposed cells. The aim of this study was to investigate induction of GI by a nongenotoxic carcinogen, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Mouse embryonic fibroblasts (C3H10T1/2) were exposed to 1, 10 or 100 nM TCDD for 2 days. Micronuclei (MN) and expression of selected cancer-related genes were assayed both immediately and at a delayed point in time (8 days). For comparison, similar experiments were done with cadmium, a known genotoxic agent. TCDD treatment induced an elevated frequency of MN at 8 days, but not directly after the exposure. TCDD-induced alterations in gene expression were also mostly delayed, with more changes observed at 8 days than at 2 days. Exposure to cadmium produced an opposite pattern of responses, with pronounced effects immediately after exposure but no increase in MN and few gene expression changes at 8 days. Although all responses to TCDD alone were delayed, menadione-induced DNA damage (measured by the Comet assay), was found to be increased directly after a 2-day TCDD exposure, indicating that the stability of the genome was compromised already at this time point. The results suggested a flat dose-response relationship consistent with dose-response data reported for radiation-induced GI. These findings indicate that TCDD, although not directly genotoxic, induces GI, which is associated with impaired DNA damage response

Ant assemblages have darker and larger members in cold environments

Aim In ectotherms, the colour of an individual's cuticle may have important thermoregulatory and protective consequences. In cool environments, ectotherms should be darker, to maximize heat gain, and larger, to minimize heat loss. Dark colours should also predominate under high UV‐B conditions because melanin offers protection. We test these predictions in ants (Hymenoptera: Formicidae) across space and through time based on a new, spatially and temporally explicit, global‐scale combination of assemblage‐level and environmental data. Location Africa, Australia and South America. Methods We sampled ant assemblages (n = 274) along 14 elevational transects on three continents. Individual assemblages ranged from 250 to 3000 m a.s.l. (minimum to maximum range in summer temperature of 0.5–35 °C). We used mixed‐effects models to explain variation in assemblage cuticle lightness. Explanatory variables were average assemblage body size, temperature and UV‐B irradiation. Annual temporal changes in lightness were examined for a subset of the data. Results Assemblages with large average body sizes were darker in colour than those with small body sizes. Assemblages became lighter in colour with increasing temperature, but darkened again at the highest temperatures when there were high levels of UV‐B. Through time, temperature and body size explained variation in lightness. Both the spatial and temporal models explained c. 50% of the variation in lightness. Main conclusions Our results are consistent with the thermal melanism hypothesis, and demonstrate the importance of considering body size and UV‐B radiation exposure in explaining the colour of insect cuticle. Crucially, this finding is at the assemblage level. Consequently, the relative abundances and identities of ant species that are present in an assemblage can change in accordance with environmental conditions over elevation, latitude and relatively short time spans. These findings suggest that there are important constraints on how ectotherm assemblages may be able to respond to rapidly changing environmental conditions

Thermoregulatory traits combine with range shifts to alter the future of montane ant assemblages

Predicting and understanding the biological response to future climate change is a pressing challenge for humanity. In the 21st century, many species will move into higher latitudes and higher elevations as the climate warms. In addition, the relative abundances of species within local assemblages are likely to change. Both effects have implications for how ecosystems function. Few biodiversity forecasts, however, take account of both shifting ranges and changing abundances. We provide a novel analysis predicting the potential changes to assemblage‐level relative abundances in the 21st century. We use an established relationship linking ant abundance and their colour and size traits to temperature and UV‐B to predict future abundance changes. We also predict future temperature driven range shifts and use these to alter the available species pool for our trait‐mediated abundance predictions. We do this across three continents under a low greenhouse gas emissions scenario (RCP2.6) and a business‐as‐usual scenario (RCP8.5). Under RCP2.6, predicted changes to ant assemblages by 2100 are moderate. On average, species richness will increase by 26%, while species composition and relative abundance structure will be 26% and 30% different, respectively, compared with modern assemblages. Under RCP8.5, however, highland assemblages face almost a tripling of species richness and compositional and relative abundance changes of 66% and 77%. Critically, we predict that future assemblages could be reorganized in terms of which species are common and which are rare: future highland assemblages will not simply comprise upslope shifts of modern lowland assemblages. These forecasts reveal the potential for radical change to montane ant assemblages by the end of the 21st century if temperature increases continue. Our results highlight the importance of incorporating trait–environment relationships into future biodiversity predictions. Looking forward, the major challenge is to understand how ecosystem processes will respond to compositional and relative abundance changes.Australian Research Council, Grant/Award Number: DP120100781; University of Pretoria; Leverhulme Trust; NERC; DST‐NRF CIB.http://wileyonlinelibrary.com/journal/gcb2020-06-01hj2019Zoology and Entomolog

A Conceptual Model of Natural and Anthropogenic Drivers and Their Influence on the Prince William Sound, Alaska, Ecosystem

Prince William Sound (PWS) is a semi-enclosed fjord estuary on the coast of Alaska adjoining the northern Gulf of Alaska (GOA). PWS is highly productive and diverse, with primary productivity strongly coupled to nutrient dynamics driven by variability in the climate and oceanography of the GOA and North Pacific Ocean. The pelagic and nearshore primary productivity supports a complex and diverse trophic structure, including large populations of forage and large fish that support many species of marine birds and mammals. High intra-annual, inter-annual, and interdecadal variability in climatic and oceanographic processes as drives high variability in the biological populations. A risk-based conceptual ecosystem model (CEM) is presented describing the natural processes, anthropogenic drivers, and resultant stressors that affect PWS, including stressors caused by the Great Alaska Earthquake of 1964 and the Exxon Valdez oil spill of 1989. A trophodynamic model incorporating PWS valued ecosystem components is integrated into the CEM. By representing the relative strengths of driver/stressors/effects, the CEM graphically demonstrates the fundamental dynamics of the PWS ecosystem, the natural forces that control the ecological condition of the Sound, and the relative contribution of natural processes and human activities to the health of the ecosystem. The CEM illustrates the dominance of natural processes in shaping the structure and functioning of the GOA and PWS ecosystems

Cerebrospinal fluid sodium rhythms

Background: Cerebrospinal fluid (CSF) sodium levels have been reported to rise during episodic migraine. Since migraine frequently starts in early morning or late afternoon, we hypothesized that natural sodium chronobiology may predispose susceptible persons when extracellular CSF sodium increases. Since no mammalian brain sodium rhythms are known, we designed a study of healthy humans to test if cation rhythms exist in CSF. Methods: Lumbar CSF was collected every ten minutes at 0.1 mL/min for 24 h from six healthy participants. CSF sodium and potassium concentrations were measured by ion chromatography, total protein by fluorescent spectrometry, and osmolarity by freezing point depression. We analyzed cation and protein distributions over the 24 h period and spectral and permutation tests to identify significant rhythms. We applied the False Discovery Rate method to adjust significance levels for multiple tests and Spearman correlations to compare sodium fluctuations with potassium, protein, and osmolarity. Results: The distribution of sodium varied much more than potassium, and there were statistically significant rhythms at 12 and 1.65 h periods. Curve fitting to the average time course of the mean sodium of all six subjects revealed the lowest sodium levels at 03.20 h and highest at 08.00 h, a second nadir at 09.50 h and a second peak at 18.10 h. Sodium levels were not correlated with potassium or protein concentration, or with osmolarity. Conclusion: These CSF rhythms are the first reports of sodium chronobiology in the human nervous system. The results are consistent with our hypothesis that rising levels of extracellular sodium may contribute to the timing of migraine onset. The physiological importance of sodium in the nervous system suggests that these rhythms may have additional repercussions on ultradian functions

Increased Frequencies of Th22 Cells as well as Th17 Cells in the Peripheral Blood of Patients with Ankylosing Spondylitis and Rheumatoid Arthritis

<div><h3>Background</h3><p>T-helper (Th) 22 is involved in the pathogenesis of inflammatory diseases. The roles of Th22 cells in the pathophysiological of ankylosing spondylitis (AS) and rheumatoid arthritis (RA) remain unsettled. So we examined the frequencies of Th22 cells, Th17 cells and Th1 cells in peripheral blood (PB) from patients with AS and patients with RA compared with both healthy controls as well as patients with osteoarthritis.</p> <h3>Design and Methods</h3><p>We studied 32 AS patients, 20 RA patients, 10 OA patients and 20 healthy controls. The expression of IL-22, IL-17 and IFN-γ were examined in AS, RA, OA patients and healthy controls by flow cytometry. Plasma IL-22 and IL-17 levels were examined by enzyme-linked immunosorbent assay.</p> <h3>Results</h3><p>Th22 cells, Th17 cells and interleukin-22 were significantly elevated in AS and RA patients compared with OA patients and healthy controls. Moreover, Th22 cells showed positive correlation with Th17 cells as well as interleukin-22 in AS and RA patients. However, positive correlation between IL-22 and Th17 cells was only found in AS patients not in RA patients. In addition, the percentages of both Th22 cells and Th17 cells correlated positively with disease activity only in RA patients not in AS patients.</p> <h3>Conclusions</h3><p>The frequencies of both Th22 cells and Th17 cells were elevated in PB from patients with AS and patients with RA. These findings suggest that Th22 cells and Th17 cells may be implicated in the pathogenesis of AS and RA, and Th22 cells and Th17 cells may be reasonable cellular targets for therapeutic intervention.</p> </div

Growth of a human mammary tumor cell line is blocked by galangin, a naturally occurring bioflavonoid, and is accompanied by down-regulation of cyclins D3, E, and A

INTRODUCTION: This study was designed to determine if and how a non-toxic, naturally occurring bioflavonoid, galangin, affects proliferation of human mammary tumor cells. Our previous studies demonstrated that, in other cell types, galangin is a potent inhibitor of the aryl hydrocarbon receptor (AhR), an environmental carcinogen-responsive transcription factor implicated in mammary tumor initiation and growth control. Because some current breast cancer therapeutics are ineffective in estrogen receptor (ER) negative tumors and since the AhR may be involved in breast cancer proliferation, the effects of galangin on the proliferation of an ER(-), AhR(high )line, Hs578T, were studied. METHODS: AhR expression and function in the presence or absence of galangin, a second AhR inhibitor, α-naphthoflavone (α-NF), an AhR agonist, indole-3-carbinol, and a transfected AhR repressor-encoding plasmid (FhAhRR) were studied in Hs578T cells by western blotting for nuclear (for instance, constitutively activated) AhR and by transfection of an AhR-driven reporter construct, pGudLuc. The effects of these agents on cell proliferation were studied by (3)H-thymidine incorporation and by flow cytometry. The effects on cyclins implicated in mammary tumorigenesis were evaluated by western blotting. RESULTS: Hs578T cells were shown to express high levels of constitutively active AhR. Constitutive and environmental chemical-induced AhR activity was profoundly suppressed by galangin as was cell proliferation. However, the failure of α-NF or FhAhRR transfection to block proliferation indicated that galangin-mediated AhR inhibition was either insufficient or unrelated to its ability to significantly block cell proliferation at therapeutically relevant doses (IC(50 )= 11 μM). Galangin inhibited transition of cells from the G(0)/G(1 )to the S phases of cell growth, likely through the nearly total elimination of cyclin D3. Expression of cyclins A and E was also suppressed. CONCLUSION: Galangin is a strong inhibitor of Hs578T cell proliferation that likely mediates this effect through a relatively unique mechanism, suppression of cyclin D3, and not through the AhR. The results suggest that this non-toxic bioflavonoid may be useful as a chemotherapeutic, particularly in combination with agents that target other components of the tumor cell cycle and in situations where estrogen receptor-specific therapeutics are ineffective