Contrasting effects of hemiparasites on ecosystem processes: can positive litter effects offset the negative effects of parasitism?

Hemiparasites are known to influence community structure and ecosystem functioning, but the underlying mechanisms are not well studied. Variation in the impacts of hemiparasites on diversity and production could be due to the difference in the relative strength of two interacting pathways: direct negative effects of parasitism and positive effects on N availability via litter. Strong effects of parasitism should result in substantial changes in diversity and declines in productivity. Conversely, strong litter effects should result in minor changes in diversity and increased productivity. We conducted field-based surveys to determine the association of Castillejaoccidentalis with diversity and productivity in the alpine tundra. To examine litter effects, we compared the decomposition of Castilleja litter with litter of four other abundant plant species, and examined the decomposition of those four species when mixed with Castilleja. Castilleja was associated with minor changes in diversity but almost a twofold increase in productivity and greater foliar N in co-occurring species. Our decomposition trials suggest litter effects are due to both the rapid N loss of Castilleja litter and the effects of mixing Castilleja litter with co-occurring species. Castilleja produces litter that accelerates decomposition in the alpine tundra, which could accelerate the slow N cycle and boost productivity. We speculate that these positive effects of litter outweigh the effects of parasitism in nutrient-poor systems with long-lived hemiparasites. Determining the relative importance of parasitism and litter effects of this functional group is crucial to understand the strong but variable roles hemiparasites play in affecting community structure and ecosystem processes

An apoptosis targeted stimulus with nanosecond pulsed electric fields (nsPEFs) in E4 squamous cell carcinoma

Stimuli directed towards activation of apoptosis mechanisms are an attractive approach to eliminate evasion of apoptosis, a ubiquitous cancer hallmark. In these in vitro studies, kinetics and electric field thresholds for several apoptosis characteristics are defined in E4 squamous carcinoma cells (SCC) exposed to ten 300 ns pulses with increasing electric fields. Cell death was >95% at the highest electric field and coincident with phosphatidylserine externalization, caspase and calpain activation in the presence and absence of cytochrome c release, decreases in Bid and mitochondria membrane potential (Δψm) without apparent changes reactive oxygen species levels or in Bcl2 and Bclxl levels. Bid cleavage was caspase-dependent (55–60%) and calcium-dependent (40–45%). Intracellular calcium as an intrinsic mechanism and extracellular calcium as an extrinsic mechanism were responsible for about 30 and 70% of calcium dependence for Bid cleavage, respectively. The results reveal electric field-mediated cell death induction and progression, activating pro-apoptotic-like mechanisms and affecting plasma membrane and intracellular functions, primarily through extrinsic-like pathways with smaller contributions from intrinsic-like pathways. Nanosecond second pulsed electric fields trigger heterogeneous cell death mechanisms in E4 SCC populations to delete them, with caspase-associated cell death as a predominant, but not an unaccompanied event

Housing Arrangement and Location Determine the Likelihood of Housing Loss Due to Wildfire

Surging wildfires across the globe are contributing to escalating residential losses and have major social, economic, and ecological consequences. The highest losses in the U.S. occur in southern California, where nearly 1000 homes per year have been destroyed by wildfires since 2000. Wildfire risk reduction efforts focus primarily on fuel reduction and, to a lesser degree, on house characteristics and homeowner responsibility. However, the extent to which land use planning could alleviate wildfire risk has been largely missing from the debate despite large numbers of homes being placed in the most hazardous parts of the landscape. Our goal was to examine how housing location and arrangement affects the likelihood that a home will be lost when a wildfire occurs. We developed an extensive geographic dataset of structure locations, including more than 5500 structures that were destroyed or damaged by wildfire since 2001, and identified the main contributors to property loss in two extensive, fire-prone regions in southern California. The arrangement and location of structures strongly affected their susceptibility to wildfire, with property loss most likely at low to intermediate structure densities and in areas with a history of frequent fire. Rates of structure loss were higher when structures were surrounded by wildland vegetation, but were generally higher in herbaceous fuel types than in higher fuel-volume woody types. Empirically based maps developed using housing pattern and location performed better in distinguishing hazardous from non-hazardous areas than maps based on fuel distribution. The strong importance of housing arrangement and location indicate that land use planning may be a critical tool for reducing fire risk, but it will require reliable delineations of the most hazardous locations

The Temporal Signature of Memories: Identification of a General Mechanism for Dynamic Memory Replay in Humans

Reinstatement of dynamic memories requires the replay of neural patterns that unfold over time in a similar manner as during perception. However, little is known about the mechanisms that guide such a temporally structured replay in humans, because previous studies used either unsuitable methods or paradigms to address this question. Here, we overcome these limitations by developing a new analysis method to detect the replay of temporal patterns in a paradigm that requires participants to mentally replay short sound or video clips. We show that memory reinstatement is accompanied by a decrease of low-frequency (8 Hz) power, which carries a temporal phase signature of the replayed stimulus. These replay effects were evident in the visual as well as in the auditory domain and were localized to sensory-specific regions. These results suggest low-frequency phase to be a domain-general mechanism that orchestrates dynamic memory replay in humans

Loss of Metal Ions, Disulfide Reduction and Mutations Related to Familial ALS Promote Formation of Amyloid-Like Aggregates from Superoxide Dismutase

Mutations in the gene encoding Cu-Zn superoxide dismutase (SOD1) are one of the causes of familial amyotrophic lateral sclerosis (FALS). Fibrillar inclusions containing SOD1 and SOD1 inclusions that bind the amyloid-specific dye thioflavin S have been found in neurons of transgenic mice expressing mutant SOD1. Therefore, the formation of amyloid fibrils from human SOD1 was investigated. When agitated at acidic pH in the presence of low concentrations of guanidine or acetonitrile, metalated SOD1 formed fibrillar material which bound both thioflavin T and Congo red and had circular dichroism and infrared spectra characteristic of amyloid. While metalated SOD1 did not form amyloid-like aggregates at neutral pH, either removing metals from SOD1 with its intramolecular disulfide bond intact or reducing the intramolecular disulfide bond of metalated SOD1 was sufficient to promote formation of these aggregates. SOD1 formed amyloid-like aggregates both with and without intermolecular disulfide bonds, depending on the incubation conditions, and a mutant SOD1 lacking free sulfhydryl groups (AS-SOD1) formed amyloid-like aggregates at neutral pH under reducing conditions. ALS mutations enhanced the ability of disulfide-reduced SOD1 to form amyloid-like aggregates, and apo-AS-SOD1 formed amyloid-like aggregates at pH 7 only when an ALS mutation was also present. These results indicate that some mutations related to ALS promote formation of amyloid-like aggregates by facilitating the loss of metals and/or by making the intramolecular disulfide bond more susceptible to reduction, thus allowing the conversion of SOD1 to a form that aggregates to form resembling amyloid. Furthermore, the occurrence of amyloid-like aggregates per se does not depend on forming intermolecular disulfide bonds, and multiple forms of such aggregates can be produced from SOD1

Differing patterns of selection and geospatial genetic diversity within two leading Plasmodium vivax candidate vaccine antigens

Although Plasmodium vivax is a leading cause of malaria around the world, only a handful of vivax antigens are being studied for vaccine development. Here, we investigated genetic signatures of selection and geospatial genetic diversity of two leading vivax vaccine antigens--Plasmodium vivax merozoite surface protein 1 (pvmsp-1) and Plasmodium vivax circumsporozoite protein (pvcsp). Using scalable next-generation sequencing, we deep-sequenced amplicons of the 42 kDa region of pvmsp-1 (n = 44) and the complete gene of pvcsp (n = 47) from Cambodian isolates. These sequences were then compared with global parasite populations obtained from GenBank. Using a combination of statistical and phylogenetic methods to assess for selection and population structure, we found strong evidence of balancing selection in the 42 kDa region of pvmsp-1, which varied significantly over the length of the gene, consistent with immune-mediated selection. In pvcsp, the highly variable central repeat region also showed patterns consistent with immune selection, which were lacking outside the repeat. The patterns of selection seen in both genes differed from their P. falciparum orthologs. In addition, we found that, similar to merozoite antigens from P. falciparum malaria, genetic diversity of pvmsp-1 sequences showed no geographic clustering, while the non-merozoite antigen, pvcsp, showed strong geographic clustering. These findings suggest that while immune selection may act on both vivax vaccine candidate antigens, the geographic distribution of genetic variability differs greatly between these two genes. The selective forces driving this diversification could lead to antigen escape and vaccine failure. Better understanding the geographic distribution of genetic variability in vaccine candidate antigens will be key to designing and implementing efficacious vaccines