Wildfire responses to abrupt climate change in North America

It is widely accepted, based on data from the last few decades and on model simulations, that anthropogenic climate change will cause increased fire activity. However, less attention has been paid to the relationship between abrupt climate changes and heightened fire activity in the paleorecord. We use 35 charcoal and pollen records to assess how fire regimes in North America changed during the last glacial–interglacial transition (15 to 10 ka), a time of large and rapid climate changes. We also test the hypothesis that a comet impact initiated continental-scale wildfires at 12.9 ka; the data do not support this idea, nor are continent-wide fires indicated at any time during deglaciation. There are, however, clear links between large climate changes and fire activity. Biomass burning gradually increased from the glacial period to the beginning of the Younger Dryas. Although there are changes in biomass burning during the Younger Dryas, there is no systematic trend. There is a further increase in biomass burning after the Younger Dryas. Intervals of rapid climate change at 13.9, 13.2, and 11.7 ka are marked by large increases in fire activity. The timing of changes in fire is not coincident with changes in human population density or the timing of the extinction of the megafauna. Although these factors could have contributed to fire-regime changes at individual sites or at specific times, the charcoal data indicate an important role for climate, and particularly rapid climate change, in determining broad-scale levels of fire activity.

4-Hydroxynonenal, an endogenous aldehyde, causes pain and neurogenic inflammation through activation of the irritant receptor TRPA1

TRPA1 is an excitatory ion channel expressed by a subpopulation of primary afferent somatosensory neurons that contain substance P and calcitonin gene-related peptide. Environmental irritants such as mustard oil, allicin, and acrolein activate TRPA1, causing acute pain, neuropeptide release, and neurogenic inflammation. Genetic studies indicate that TRPA1 is also activated downstream of one or more proalgesic agents that stimulate phospholipase C signaling pathways, thereby implicating this channel in peripheral mechanisms controlling pain hypersensitivity. However, it is not known whether tissue injury also produces endogenous proalgesic factors that activate TRPA1 directly to augment inflammatory pain. Here, we report that recombinant or native TRPA1 channels are activated by 4-hydroxy-2-nonenal (HNE), an endogenous alpha,beta-unsaturated aldehyde that is produced when reactive oxygen species peroxidate membrane phospholipids in response to tissue injury, inflammation, and oxidative stress. HNE provokes release of substance P and calcitonin gene-related peptide from central (spinal cord) and peripheral (esophagus) nerve endings, resulting in neurogenic plasma protein extravasation in peripheral tissues. Moreover, injection of HNE into the rodent hind paw elicits pain-related behaviors that are inhibited by TRPA1 antagonists and absent in animals lacking functional TRPA1 channels. These findings demonstrate that HNE activates TRPA1 on nociceptive neurons to promote acute pain, neuropeptide release, and neurogenic inflammation. Our results also provide a mechanism-based rationale for developing novel analgesic or anti-inflammatory agents that target HNE production or TRPA1 activation.

Enhanced hepatitis C virus genome replication and lipid accumulation mediated by inhibition of AMP-activated protein kinase

Hepatitis C virus (HCV) infection is associated with dysregulation of both lipid and glucose metabolism. As well as contributing to viral replication, these perturbations influence the pathogenesis associated with the virus, including steatosis, insulin resistance, and type 2 diabetes. AMP-activated protein kinase (AMPK) plays a key role in regulation of both lipid and glucose metabolism. We show here that, in cells either infected with HCV or harboring an HCV subgenomic replicon, phosphorylation of AMPK at threonine 172 and concomitant AMPK activity are dramatically reduced. We demonstrate that this effect is mediated by activation of the serine/threonine kinase, protein kinase B, which inhibits AMPK by phosphorylating serine 485. The physiological significance of this inhibition is demonstrated by the observation that pharmacological restoration of AMPK activity not only abrogates the lipid accumulation observed in virus-infected and subgenomic replicon-harboring cells but also efficiently inhibits viral replication. These data demonstrate that inhibition of AMPK is required for HCV replication and that the restoration of AMPK activity may present a target for much needed anti-HCV therapies.

Suppression of a pro-apoptotic K+ channel as a mechanism for hepatitis C virus persistence

An estimated 3% of the global population are infected with hepatitis C virus (HCV), and the majority of these individuals will develop chronic liver disease. As with other chronic viruses, establishment of persistent infection requires that HCV-infected cells must be refractory to a range of pro-apoptotic stimuli. In response to oxidative stress, amplification of an outward K(+) current mediated by the Kv2.1 channel, precedes the onset of apoptosis. We show here that in human hepatoma cells either infected with HCV or harboring an HCV subgenomic replicon, oxidative stress failed to initiate apoptosis via Kv2.1. The HCV NS5A protein mediated this effect by inhibiting oxidative stress-induced p38 MAPK phosphorylation of Kv2.1. The inhibition of a host cell K(+) channel by a viral protein is a hitherto undescribed viral anti-apoptotic mechanism and represents a potential target for antiviral therapy.

The maximum rate of mammal evolution

How fast can a mammal evolve from the size of a mouse to the size of an elephant? Achieving such a large transformation calls for major biological reorganization. Thus, the speed at which this occurs has important implications for extensive faunal changes, including adaptive radiations and recovery from mass extinctions. To quantify the pace of large-scale evolution we developed a metric, clade maximum rate, which represents the maximum evolutionary rate of a trait within a clade. We applied this metric to body mass evolution in mammals over the last 70 million years, during which multiple large evolutionary transitions occurred in oceans and on continents and islands. Our computations suggest that it took a minimum of 1.6, 5.1, and 10 million generations for terrestrial mammal mass to increase 100-, and 1,000-, and 5,000- fold, respectively. Values for whales were down to half the length (i.e., 1.1, 3, and 5 million generations), perhaps due to the reduced mechanical constraints of living in an aquatic environment. When differences in generation time are considered, we find an exponential increase in maximum mammal body mass during the 35 million years following the Cretaceous–Paleogene (K–Pg) extinction event. Our results also indicate a basic asymmetry in macroevolution: very large decreases (such as extreme insular dwarfism) can happen at more than 10 times the rate of increases. Our findings allow more rigorous comparisons of microevolutionary and macroevolutionary patterns and processes. Keywords: haldanes, biological time, scaling, pedomorphosis

Phosphorylation of the voltage-gated potassium channel Kv2.1 by AMP-activated protein kinase regulates membrane excitability

Firing of action potentials in excitable cells accelerates ATP turnover. The voltage-gated potassium channel Kv2.1 regulates action potential frequency in central neurons, whereas the ubiquitous cellular energy sensor AMP-activated protein kinase (AMPK) is activated by ATP depletion and protects cells by switching off energy-consuming processes. We show that treatment of HEK293 cells expressing Kv2.1 with the AMPK activator A-769662 caused hyperpolarizing shifts in the current-voltage relationship for channel activation and inactivation. We identified two sites (S440 and S537) directly phosphorylated on Kv2.1 by AMPK and, using phosphospecific antibodies and quantitative mass spectrometry, show that phosphorylation of both sites increased in A-769662-treated cells. Effects of A-769662 were abolished in cells expressing Kv2.1 with S440A but not with S537A substitutions, suggesting that phosphorylation of S440 was responsible for these effects. Identical shifts in voltage gating were observed after introducing into cells, via the patch pipette, recombinant AMPK rendered active but phosphatase-resistant by thiophosphorylation. Ionomycin caused changes in Kv2.1 gating very similar to those caused by A-769662 but acted via a different mechanism involving Kv2.1 dephosphorylation. In cultured rat hippocampal neurons, A-769662 caused hyperpolarizing shifts in voltage gating similar to those in HEK293 cells, effects that were abolished by intracellular dialysis with Kv2.1 antibodies. When active thiophosphorylated AMPK was introduced into cultured neurons via the patch pipette, a progressive, time-dependent decrease in the frequency of evoked action potentials was observed. Our results suggest that activation of AMPK in neurons during conditions of metabolic stress exerts a protective role by reducing neuronal excitability and thus conserving energy.

Unconscious effects of language-specific terminology on pre-attentive colour perception

It is now established that native language affects one's perception of the world. However, it is unknown whether this effect is merely driven by conscious, language-based evaluation of the environment or whether it reflects fundamental differences in perceptual processing between individuals speaking different languages. Using brain potentials, we demonstrate that the existence in Greek of 2 color terms—ghalazio and ble—distinguishing light and dark blue leads to greater and faster perceptual discrimination of these colors in native speakers of Greek than in native speakers of English. The visual mismatch negativity, an index of automatic and preattentive change detection, was similar for blue and green deviant stimuli during a color oddball detection task in English participants, but it was significantly larger for blue than green deviant stimuli in native speakers of Greek. These findings establish an implicit effect of language-specific terminology on human color perception.

Late Pleistocene climate change and the global expansion of anatomically modern humans

The extent to which past climate change has dictated the pattern and timing of the out-of-Africa expansion by anatomically modern humans is currently unclear [Stewart JR, Stringer CB (2012) Science 335:1317–1321]. In particular, the incompleteness of the fossil record makes it difficult to quantify the effect of climate. Here, we take a different approach to this problem; rather than relying on the appearance of fossils or archaeological evidence to determine arrival times in different parts of the world, we use patterns of genetic variation in modern human populations to determine the plausibility of past demographic parameters. We develop a spatially explicit model of the expansion of anatomically modern humans and use climate reconstructions over the past 120 ky based on the Hadley Centre global climate model HadCM3 to quantify the possible effects of climate on human demography. The combinations of demographic parameters compatible with the current genetic makeup of worldwide populations indicate a clear effect of climate on past population densities. Our estimates of this effect, based on population genetics, capture the observed relationship between current climate and population density in modern hunter–gatherers worldwide, providing supporting evidence for the realism of our approach. Furthermore, although we did not use any archaeological and anthropological data to inform the model, the arrival times in different continents predicted by our model are also broadly consistent with the fossil and archaeological records. Our framework provides the most accurate spatiotemporal reconstruction of human demographic history available at present and will allow for a greater integration of genetic and archaeological evidence.

Neural correlates of cognitive dissonance and choice-induced preference change

According to many modern economic theories, actions simply reflect an individual's preferences, whereas a psychological phenomenon called “cognitive dissonance” claims that actions can also create preference. Cognitive dissonance theory states that after making a difficult choice between two equally preferred items, the act of rejecting a favorite item induces an uncomfortable feeling (cognitive dissonance), which in turn motivates individuals to change their preferences to match their prior decision (i.e., reducing preference for rejected items). Recently, however, Chen and Risen [Chen K, Risen J (2010) J Pers Soc Psychol 99:573–594] pointed out a serious methodological problem, which casts a doubt on the very existence of this choice-induced preference change as studied over the past 50 y. Here, using a proper control condition and two measures of preferences (self-report and brain activity), we found that the mere act of making a choice can change self-report preference as well as its neural representation (i.e., striatum activity), thus providing strong evidence for choice-induced preference change. Furthermore, our data indicate that the anterior cingulate cortex and dorsolateral prefrontal cortex tracked the degree of cognitive dissonance on a trial-by-trial basis. Our findings provide important insights into the neural basis of how actions can alter an individual's preferences.

Neural basis of the undermining effect of monetary reward on intrinsic motivation

Contrary to the widespread belief that people are positively motivated by reward incentives, some studies have shown that performance-based extrinsic reward can actually undermine a person's intrinsic motivation to engage in a task. This “undermining effect” has timely practical implications, given the burgeoning of performance-based incentive systems in contemporary society. It also presents a theoretical challenge for economic and reinforcement learning theories, which tend to assume that monetary incentives monotonically increase motivation. Despite the practical and theoretical importance of this provocative phenomenon, however, little is known about its neural basis. Herein we induced the behavioral undermining effect using a newly developed task, and we tracked its neural correlates using functional MRI. Our results show that performance-based monetary reward indeed undermines intrinsic motivation, as assessed by the number of voluntary engagements in the task. We found that activity in the anterior striatum and the prefrontal areas decreased along with this behavioral undermining effect. These findings suggest that the corticobasal ganglia valuation system underlies the undermining effect through the integration of extrinsic reward value and intrinsic task value.

Which of satellite- or model-based estimates is closer to reality for aerosol indirect forcing?

In their contribution to PNAS, Penner et al. (1) used a climate model to estimate the radiative forcing by the aerosol first indirect effect (cloud albedo effect) in two different ways: first, by deriving a statistical relationship between the logarithm of cloud droplet number concentration, ln Nc, and the logarithm of aerosol optical depth, ln AOD (or the logarithm of the aerosol index, ln AI) for present-day and preindustrial aerosol fields, a method that was applied earlier to satellite data (2), and, second, by computing the radiative flux perturbation between two simulations with and without anthropogenic aerosol sources. They find a radiative forcing that is a factor of 3 lower in the former approach than in the latter [as Penner et al. (1) correctly noted, only their “inline” results are useful for the comparison]. This study is a very interesting contribution, but we believe it deserves several clarifications.

Cox-dependent fatty acid metabolites cause pain through activation of the irritant receptor TRPA1.

Prostaglandins (PG) are known to induce pain perception indirectly by sensitizing nociceptors. Accordingly, the analgesic action of nonsteroidal anti-inflammatory drugs (NSAIDs) results from inhibition of cyclooxygenases and blockade of PG biosynthesis. Cyclopentenone PGs, 15-d-PGJ(2), PGA(2), and PGA(1), formed by dehydration of their respective parent PGs, PGD(2), PGE(2), and PGE(1), possess a highly reactive alpha,beta-unsaturated carbonyl group that has been proposed to gate the irritant transient receptor potential A1 (TRPA1) channel. Here, by using TRPA1 wild-type (TRPA1(+/+)) or deficient (TRPA1(-/-)) mice, we show that cyclopentenone PGs produce pain by direct stimulation of nociceptors via TRPA1 activation. Cyclopentenone PGs caused a robust calcium response in dorsal root ganglion (DRG) neurons of TRPA1(+/+), but not of TRPA1(-/-) mice, and a calcium-dependent release of sensory neuropeptides from the rat dorsal spinal cord. Intraplantar injection of cyclopentenone PGs stimulated c-fos expression in spinal neurons of the dorsal horn and evoked an instantaneous, robust, and transient nociceptive response in TRPA1(+/+) but not in TRPA1(-/-) mice. The classical proalgesic PG, PGE(2), caused a slight calcium response in DRG neurons, increased c-fos expression in spinal neurons, and induced a delayed and sustained nociceptive response in both TRPA1(+/+) and TRPA1(-/-) mice. These results expand the mechanism of NSAID analgesia from blockade of indirect nociceptor sensitization by classical PGs to inhibition of direct TRPA1-dependent nociceptor activation by cyclopentenone PGs. Thus, TRPA1 antagonism may contribute to suppress pain evoked by PG metabolites without the adverse effects of inhibiting cyclooxygenases.

Governance, agricultural intensification and land sparing in tropical South America

In this paper we address two topical questions: How do the quality of governance and agricultural intensification impact on spatial expansion of agriculture? Which aspects of governance are more likely to ensure that agricultural intensification allows sparing land for nature? Using data from the Food and Agriculture Organization, the World Bank, the World Database on Protected Areas, and the Yale Center for Environmental Law and Policy, we estimate a panel data model for six South American countries and quantify the effects of major determinants of agricultural land expansion, including various dimensions of governance, over the period 1970–2006. The results indicate that the effect of agricultural intensification on agricultural expansion is conditional on the quality and type of governance. When considering conventional aspects of governance, agricultural intensification leads to an expansion of agricultural area when governance scores are high. When looking specifically at environmental aspects of governance, intensification leads to a spatial contraction of agriculture when governance scores are high, signaling a sustainable intensification process.

Environmental impact of geometric earthwork construction in pre-Columbian Amazonia

There is considerable controversy over whether pre-Columbian (pre-A.D. 1492) Amazonia was largely “pristine” and sparsely populated by slash-and-burn agriculturists, or instead a densely populated, domesticated landscape, heavily altered by extensive deforestation and anthropogenic burning. The discovery of hundreds of large geometric earthworks beneath intact rainforest across southern Amazonia challenges its status as a pristine landscape, and has been assumed to indicate extensive pre-Columbian deforestation by large populations. We tested these assumptions using coupled local- and regional-scale paleoecological records to reconstruct land use on an earthwork site in northeast Bolivia within the context of regional, climate-driven biome changes. This approach revealed evidence for an alternative scenario of Amazonian land use, which did not necessitate labor-intensive rainforest clearance for earthwork construction. Instead, we show that the inhabitants exploited a naturally open savanna landscape that they maintained around their settlement despite the climatically driven rainforest expansion that began ∼2,000 y ago across the region. Earthwork construction and agriculture on terra firme landscapes currently occupied by the seasonal rainforests of southern Amazonia may therefore not have necessitated large-scale deforestation using stone tools. This finding implies far less labor—and potentially lower population density—than previously supposed. Our findings demonstrate that current debates over the magnitude and nature of pre-Columbian Amazonian land use, and its impact on global biogeochemical cycling, are potentially flawed because they do not consider this land use in the context of climate-driven forest–savanna biome shifts through the mid-to-late Holocene.