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The complex nature of growth and decomposition in microbial mats results in a broad range of microbial preservation. Such taphonomic variability complicates both the description of microbial elements preserved within geologic materials and the potential interpretation of microbial biomarkers. This study uses a taphonomic assessment to explore the preservation of different microbial components within silicified microbial mats of the late Mesoproterozoic (~1.0 Ga) Angmaat Formation, Bylot Supergroup, Baffin Island. The Angmaat Formation consists of unmetamorphosed and essentially undeformed strata that represent intertidal to supratidal deposition within an evaporative microbial flat. Early diagenetic silicification preserved microbial communities across a range of environments, from those episodically exposed to persistently submerged. Here, we present the development of a new methodology involving the use of high-resolution image mosaics to investigate the taphonomy of microfossils preserved in these mats. A taphonomic grade is assigned using a modified classification that accounts for both the taphonomic preservation state (good, fair, poor) of individual microfossils, as well as the degree of compaction of the overall mat. We show that although various taphonomic states occur within each of the silicified mats, the overall taphonomic assessment differentiates between well-preserved mats that are interpreted to have been silicified during active growth, to highly degraded and compacted mats that are interpreted to represent preservation during later stages of biological decomposition. These data indicate that even small changes in the timing of silicification may have substantial implications on our identification of microbial biomarkers and, therefore, our interpretation of early Earth ecosystems.

Air exchange through infiltration is driven partly by indoor/outdoor temperature differences, and as climate change increases ambient temperatures, such differences could vary considerably even with small ambient temperature increments, altering patterns of exposures to both indoor and outdoor pollutants. We calculated changes in air fluxes through infiltration for prototypical detached homes in nine metropolitan areas in the United States (Atlanta, Boston, Chicago, Houston, Los Angeles, Minneapolis, New York, Phoenix, and Seattle) from 1970–2000 to 2040–2070. The Lawrence Berkeley National Laboratory model of infiltration was used in combination with climate data from eight regionally downscaled climate models from the North American Regional Climate Change Assessment Program. Averaged over all study locations, seasons, and climate models, air exchange through infiltration would decrease by ~5%. Localized increased infiltration is expected during the summer months, up to 20–30%. Seasonal and daily variability in infiltration are also expected to increase, particularly during the summer months. Diminished infiltration in future climate scenarios may be expected to increase exposure to indoor sources of air pollution, unless these ventilation reductions are otherwise compensated. Exposure to ambient air pollution, conversely, could be mitigated by lower infiltration, although peak exposure increases during summer months should be considered, as well as other mechanisms.

Over the last decade, an extensive beetle outbreak has impacted western North America resulting in the mortality of over 100,000 km2 of forest throughout British Columbia and the western United States. Climate change has aided the expansion and continuation of this beetle infestation for more than a decade as beetles survive milder winters and expand northward and to higher elevation areas. Studies have been conducted to investigate the impact of this disturbance on forest carbon stocks, beetle-fire interactions, and meteorological variables, as well as to affirm the importance of including beetle infestation in models. In recent years there has been increased interest in the impact of beetle mortality and attack on atmospheric composition. Numerous studies have demonstrated that insect attack can prompt elevated emissions of volatile organic compounds (VOCs) in a variety of plant and tree species, including mountain pine beetle attacking lodgepole pine, the main beetle-host combination in the current outbreak. These enhanced VOC emissions are likely a defense mechanism of the tree, consisting of increasing emissions of compounds that are toxic to the beetles and attract predators of the beetles as well as increasing sap flow to help remove beetles from the trunk. This impact has not yet been modeled; however, beetle attack may have a significant impact on atmospheric composition and air quality in western North America. In this study, we use 14 years of beetle mortality data for 13 beetle species and beetle-induced monoterpene concentration data in the NCAR Community Earth System Model (CESM) to investigate the impact of beetle mortality and attack on monoterpene emissions and secondary organic aerosol (SOA) formation in western North America. Needleleaf vegetation is decreased each year based on the annual mortality data while emissions of certain compounds in needleleaf trees under attack are scaled-up based on recent beetle-induced VOC data for lodgepole pine (pine scenario) and Engelmann spruce (spruce scenario). As the mountain pine beetle has had the most extensive impact on mortality, we compare changes in emissions of VOCs and subsequent SOA formation caused by the mountain pine beetle to changes caused by the other 12 beetles combined. Beetle infestation impacts monoterpene emissions through both decreased emissions as trees are killed off (mortality effect) and increased emissions in trees under attack (attack effect). Regionally, beetle infestation may have a significant impact on monoterpene emissions and SOA concentrations with up to a 4-fold increase in monoterpene emissions and up to a 40% increase in SOA concentrations in some years. Responses to beetle attack can vary greatly over space and time as the areas affected as well as the magnitude of the impact depend on the extent of previous mortality and the number of trees under attack in a year. The model captures highly localized impacts on smaller-scales, while on larger-scales, the cumulative mortality effect often mutes the ongoing attack effect. The mountain pine beetle alone has an impact similar to that of the other 12 beetles combined, and the spruce scenario has an impact 3-4 times greater than the pine scenario due to differences in the magnitude of the observed enhancement in monoterpene emissions. In North America, the pine scenario would likely dominate since lodgepole pine is the main species impacted; however, smaller regions of spruce may see higher localized impacts on monoterpene emissions and SOA concentrations. Placed in the context of OM and PM2.5 IMPROVE network measurements, the changes in SOA concentrations due to beetle attack are in most cases small compared to the large annual and interannual variability in the measurements of total organic aerosol, indicating that most beetle-induced SOA changes are not likely detectable in current observation networks. However, in areas with especially large emissions enhancements (e.g. areas of spruce under attack) and lower variability in measurements of OM, beetle-induced changes in SOA may be observable. Due to the large potential impacts that beetle infestation may have on monoterpene emissions, SOA formation, and degradation of air quality, it is important that beetle infestation be included in future models.

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease of motor neurons leading to death from respiratory failure within about 3 years of symptom onset. A family history of ALS is obtained in about 5 % but the distinction between familial and apparently sporadic ALS is artificial and genetic factors play a role in all types. For several years, only one gene was known to have a role in ALS pathogenesis, SOD1 . In the last few years there has been a rapid advance in our genetic knowledge of the causes of ALS, and the relationship of the genetic subtypes with pathological subtypes and clinical phenotype. Mutations in the gene for TDP-43 protein, TARDBP , highlight this, with pathology mimicking closely that found in other types of ALS, and a phenotypic spectrum that includes frontotemporal dementia. Mutations in the FUS gene, closely related to TDP-43, lead to a similar clinical phenotype but distinct pathology, so that the three pathological groups represented by SOD1 , TARDBP , and FUS are distinct. In this review, we explore the genetic architecture of ALS, highlight some of the genes implicated in pathogenesis, and describe their phenotypic range and overlap with other diseases.

Mutations in the profilin 1 ( PFN1 ) gene, which is crucial for the conversion of monomeric to filamentous actin, can cause familial amyotrophic lateral sclerosis, suggesting that alterations in cytoskeletal pathways contribute to disease pathogenesis. Genetics of familial amyotrophic lateral sclerosis In nearly half of the familial cases of the neurodegenerative disorder amyotrophic lateral sclerosis (ALS), the genetic basis remains unknown. These authors show that mutations in the profilin 1 ( PFN1 ) gene, which is essential for the conversion of monomeric to filamentous actin, can cause familial ALS. The available data suggest that alterations in cytoskeletal pathways contribute to the pathogenesis of ALS. The observation of PFN1 mutations in ALS has immediate implications for diagnostic testing of familial ALS cases and provides a novel potential target for the treatment of ALS. Amyotrophic lateral sclerosis (ALS) is a late-onset neurodegenerative disorder resulting from motor neuron death. Approximately 10% of cases are familial (FALS), typically with a dominant inheritance mode. Despite numerous advances in recent years 1 , 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 , nearly 50% of FALS cases have unknown genetic aetiology. Here we show that mutations within the profilin 1 ( PFN1 ) gene can cause FALS. PFN1 is crucial for the conversion of monomeric (G)-actin to filamentous (F)-actin. Exome sequencing of two large ALS families showed different mutations within the PFN1 gene. Further sequence analysis identified 4 mutations in 7 out of 274 FALS cases. Cells expressing PFN1 mutants contain ubiquitinated, insoluble aggregates that in many cases contain the ALS-associated protein TDP-43. PFN1 mutants also display decreased bound actin levels and can inhibit axon outgrowth. Furthermore, primary motor neurons expressing mutant PFN1 display smaller growth cones with a reduced F/G-actin ratio. These observations further document that cytoskeletal pathway alterations contribute to ALS pathogenesis.

The relationship between food addiction, an important emerging construct of excessive eating pathology, and dietary restraint has yet to be fully understood. Eating disorder models commonly posit that dietary restraint exacerbates loss of control eating (e.g., binge episodes) and may also play a causal role in the development of food addiction. However, dietary restraint as a reaction to consequences of food addiction (e.g., uncontrollable eating or weight gain) represents another plausible pathway. Existing studies indicate that the association between food addiction and dietary restraint may be more significant during adolescence than adulthood, but are limited by cross-sectional study designs. A longitudinal study using an adolescent sample is ideal for investigating potential pathways underlying links between food addiction and dietary restraint. This study examined temporal pathways between food addiction and dietary restraint in a sample of one hundred twenty-seven adolescents (M = 14.8, SD = 1.1) at three timepoints spanning two years. This is the first study to examine longitudinal cross-lagged panel associations between food addiction and dietary restraint. In this adolescent sample, food addiction significantly predicted future dietary restraint (b = 0.25, SE = 0.06, p < 0.001), but dietary restraint did not significantly predict future food addiction (b = 0.06, SE = 0.05, p > 0.05). These findings support the theory that dietary restraint may be a reaction to deleterious effects of food addiction during adolescence.