Stressors and threats to the flora of Acadia National Park, Maine: Current knowledge, information gaps, and future directions

Stressors and threats to the flora of Acadia National Park, Maine: Current knowledge, information gaps, and future directions. J. Torrey Bot. Soc. 139: 323–344. 2012.— Acadia National Park is a center of plant diversity in northeastern North America. The Park\u27s varied habitats and flora are sensitive to a number of natural and anthropogenic perturbations. Stressors such as invasive plants, pest and pathogens, ozone, acidic fog and sulfur deposition, nitrogen deposition, heavy metals, fire and fire suppression, over-browsing, visitor use, hurricanes, and climate change have all had effects on the Park\u27s habitats and plant species at some point and it is unclear how many of these stressors are currently affecting the flora of Acadia National Park. We discuss the botanical diversity of Acadia, assess the natural and anthropogenic stressors and threats affecting the Park\u27s flora, and summarize critical information gaps to better assess the known stressors and threats to the flora. Understanding these stressors and threats is critical to making informed management decisions to preserve the botanical diversity of Acadia and other regional parks

Semantics of a Typed Algebraic Lambda-Calculus

Algebraic lambda-calculi have been studied in various ways, but their semantics remain mostly untouched. In this paper we propose a semantic analysis of a general simply-typed lambda-calculus endowed with a structure of vector space. We sketch the relation with two established vectorial lambda-calculi. Then we study the problems arising from the addition of a fixed point combinator and how to modify the equational theory to solve them. We sketch an algebraic vectorial PCF and its possible denotational interpretations

The STAFF-DWP wave instrument on the DSP equatorial spacecraft: description and first results

The STAFF-DWP wave instrument on board the equatorial spacecraft (TC1) of the Double Star Project consists of a combination of 2 instruments which are a heritage of the Cluster mission: the Spatio-Temporal Analysis of Field Fluctuations (STAFF) experiment and the Digital Wave-Processing experiment (DWP). On DSP-TC1 STAFF consists of a three-axis search coil magnetometer, used to measure magnetic fluctuations at frequencies up to 4 kHz and a waveform unit, up to 10 Hz, plus snapshots up to 180 Hz. DWP provides several onboard analysis tools: a complex FFT to fully characterise electromagnetic waves in the frequency range 10 Hz-4 kHz, a particle correlator linked to the PEACE electron experiment, and compression of the STAFF waveform data. The complementary Cluster and TC1 orbits, together with the similarity of the instruments, permits new multi-point studies. The first results show the capabilities of the experiment, with examples in the different regions of the magnetosphere-solar wind system that have been encountered by DSP-TC1 at the beginning of its operational phase. An overview of the different kinds of electromagnetic waves observed on the dayside from perigee to apogee is given, including the different whistler mode waves (hiss, chorus, lion roars) and broad-band ULF emissions. The polarisation and propagation characteristics of intense waves in the vicinity of a bow shock crossing are analysed using the dedicated PRASSADCO tool, giving results compatible with previous studies: the broad-band ULF waves consist of a superimposition of different wave modes, whereas the magnetosheath lion roars are right-handed and propagate close to the magnetic field. An example of a combined Cluster DSP-TC1 magnetopause crossing is given. This first case study shows that the ULF wave power intensity is higher at low latitude (DSP) than at high latitude (Cluster). On the nightside in the tail, a first wave event comparison - in a rather quiet time interval - is shown. It opens the doors to future studies, such as event timing during substorms, to possibly determine their onset location

Is LMNB1 a susceptibility gene for neural tube defects in humans?

BACKGROUND: Lamins are intermediate filament proteins that form a major component of the nuclear lamina, a protein complex at the surface of the inner nuclear membrane. Numerous clinically diverse conditions, termed laminopathies, have been found to result from mutation of LMNA. In contrast, coding or loss of function mutations of LMNB1, encoding lamin B1, have not been identified in human disease. In mice, polymorphism in Lmnb1 has been shown to modify risk of neural tube defects (NTDs), malformations of the central nervous system that result from incomplete closure of the neural folds. METHODS: Mutation analysis by DNA sequencing was performed on all exons of LMNB1 in 239 samples from patients with NTDs from the United Kingdom, Sweden, and United States. Possible functional effects of missense variants were analyzed by bioinformatics prediction and fluorescence in photobleaching. RESULTS: In NTD patients, we identified two unique missense variants that were predicted to disrupt protein structure/function and represent putative contributory mutations. Fluorescence loss in photobleaching analysis showed that the A436T variant compromised stability of lamin B1 interaction within the lamina. CONCLUSION: The genetic basis of human NTDs appears highly heterogenous with possible involvement of multiple predisposing genes. We hypothesize that rare variants of LMNB1 may contribute to susceptibility to NTDs. Birth Defects Research (Part A), 2013. © 2013 Wiley Periodicals, Inc

Essential versus accessory aspects of cell death: recommendations of the NCCD 2015

Cells exposed to extreme physicochemical or mechanical stimuli die in an uncontrollable manner, as a result of their immediate structural breakdown. Such an unavoidable variant of cellular demise is generally referred to as ‘accidental cell death’ (ACD). In most settings, however, cell death is initiated by a genetically encoded apparatus, correlating with the fact that its course can be altered by pharmacologic or genetic interventions. ‘Regulated cell death’ (RCD) can occur as part of physiologic programs or can be activated once adaptive responses to perturbations of the extracellular or intracellular microenvironment fail. The biochemical phenomena that accompany RCD may be harnessed to classify it into a few subtypes, which often (but not always) exhibit stereotyped morphologic features. Nonetheless, efficiently inhibiting the processes that are commonly thought to cause RCD, such as the activation of executioner caspases in the course of apoptosis, does not exert true cytoprotective effects in the mammalian system, but simply alters the kinetics of cellular demise as it shifts its morphologic and biochemical correlates. Conversely, bona fide cytoprotection can be achieved by inhibiting the transduction of lethal signals in the early phases of the process, when adaptive responses are still operational. Thus, the mechanisms that truly execute RCD may be less understood, less inhibitable and perhaps more homogeneous than previously thought. Here, the Nomenclature Committee on Cell Death formulates a set of recommendations to help scientists and researchers to discriminate between essential and accessory aspects of cell death

Field Effectiveness of Pandemic and 2009-2010 Seasonal Vaccines against 2009-2010 A(H1N1) Influenza: Estimations from Surveillance Data in France

BACKGROUND: In this study, we assess how effective pandemic and trivalent 2009-2010 seasonal vaccines were in preventing influenza-like illness (ILI) during the 2009 A(H1N1) pandemic in France. We also compare vaccine effectiveness against ILI versus laboratory-confirmed pandemic A(H1N1) influenza, and assess the possible bias caused by using non-specific endpoints and observational data. METHODOLOGY AND PRINCIPAL FINDINGS: We estimated vaccine effectiveness by using the following formula: VE  =  (PPV-PCV)/(PPV(1-PCV)) × 100%, where PPV is the proportion vaccinated in the population and PCV the proportion of vaccinated influenza cases. People were considered vaccinated three weeks after receiving a dose of vaccine. ILI and pandemic A(H1N1) laboratory-confirmed cases were obtained from two surveillance networks of general practitioners. During the epidemic, 99.7% of influenza isolates were pandemic A(H1N1). Pandemic and seasonal vaccine uptakes in the population were obtained from the National Health Insurance database and by telephonic surveys, respectively. Effectiveness estimates were adjusted by age and week. The presence of residual biases was explored by calculating vaccine effectiveness after the influenza period. The effectiveness of pandemic vaccines in preventing ILI was 52% (95% confidence interval: 30-69) during the pandemic and 33% (4-55) after. It was 86% (56-98) against confirmed influenza. The effectiveness of seasonal vaccines against ILI was 61% (56-66) during the pandemic and 19% (-10-41) after. It was 60% (41-74) against confirmed influenza. CONCLUSIONS: The effectiveness of pandemic vaccines in preventing confirmed pandemic A(H1N1) influenza on the field was high, consistently with published findings. It was significantly lower against ILI. This is unsurprising since not all ILI cases are caused by influenza. Trivalent 2009-2010 seasonal vaccines had a statistically significant effectiveness in preventing ILI and confirmed pandemic influenza, but were not better in preventing confirmed pandemic influenza than in preventing ILI. This lack of difference might be indicative of selection bias

Genetic Ablation of Bcl-x Attenuates Invasiveness without Affecting Apoptosis or Tumor Growth in a Mouse Model of Pancreatic Neuroendocrine Cancer

Tumor cell death is modulated by an intrinsic cell death pathway controlled by the pro- and anti-apoptotic members of the Bcl-2 family. Up-regulation of anti-apoptotic Bcl-2 family members has been shown to suppress cell death in pre-clinical models of human cancer and is implicated in human tumor progression. Previous gain-of-function studies in the RIP1-Tag2 model of pancreatic islet carcinogenesis, involving uniform or focal/temporal over-expression of Bcl-xL, demonstrated accelerated tumor formation and growth. To specifically assess the role of endogenous Bcl-x in regulating apoptosis and tumor progression in this model, we engineered a pancreatic β-cell-specific knockout of both alleles of Bcl-x using the Cre-LoxP system of homologous recombination. Surprisingly, there was no appreciable effect on tumor cell apoptosis rates or on tumor growth in the Bcl-x knockout mice. Other anti-apoptotic Bcl-2 family members were expressed but not substantively altered at the mRNA level in the Bcl-x-null tumors, suggestive of redundancy without compensatory transcriptional up-regulation. Interestingly, the incidence of invasive carcinomas was reduced, and tumor cells lacking Bcl-x were impaired in invasion in a two-chamber trans-well assay under conditions mimicking hypoxia. Thus, while the function of Bcl-x in suppressing apoptosis and thereby promoting tumor growth is evidently redundant, genetic ablation implicates Bcl-x in selectively facilitating invasion, consistent with a recent report documenting a pro-invasive capability of Bcl-xL upon exogenous over-expression