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Oak reproduction is characterized by mast seeding with high inter-annual fluctuations in fruit production. Such resource pulses can greatly affect ecosystem functioning and may cause seed consumers to alter their mobility, demography, or diet. Consequences of mast seeding for seed consumers remain poorly understood as their long timescale makes them difficult to study. We investigated impacts of oak mast seeding on the feeding behavior of two sympatric European deer species: red deer (Cervus elaphus) and roe deer (Capreolus capreolus). We analyzed their rumen content over a 31-year period in tandem with 10 years of data on oak fructification (i.e. 8 years of field monitoring and two modelled years). Acorn production is strongly correlated with consumption by both deer species. In years of high fructification, acorns represent more than 50% and 35% of red and roe deer diet, respectively, confirming assumptions that deer favor acorns when these are available. Red deer eat more acorns than roe deer both between and within years. High acorn production in mast years appears to saturate the capacity of deer to consume acorns. As the proportion of acorns increase in their diet, red deer eat more grasses and less conifer browse. No dietary shift was found for roe deer. By inducing dietary shifts in consumers, oak mast seeding can have cascading effects on ecosystem processes, notably on the damages on conifers caused by red deer and the consequences for forest dynamics. [ABSTRACT FROM AUTHOR]

The cultivation of Genetically Modified (GM) crops may have substantial impacts on populations of non-target organisms (NTOs) in agroecosystems. These impacts should be assessed at larger spatial scales than the cultivated field, and, as landscape-scale experiments are difficult, if not impossible, modelling approaches are needed to address landscape risk management. We present an original stochastic and spatially explicit modelling framework for assessing the risk at the landscape level. We use techniques from spatial statistics for simulating simplified landscapes made up of (aggregated or non-aggregated) GM fields, neutral fields and NTO's habitat areas. The dispersal of toxic pollen grains is obtained by convolving the emission of GM plants and validated dispersal kernel functions while the locations of exposed individuals are drawn from a point process. By taking into account the adherence of the ambient pollen on plants, the loss of pollen due to climatic events, and, an experimentally-validated mortality-dose function we predict risk maps and provide a distribution giving how the risk varies within exposed individuals in the landscape. Then, we consider the impact of the Bt maize on Inachis io in worst-case scenarii where exposed individuals are located in the vicinity of GM fields and pollen shedding overlaps with larval emergence. We perform a Global Sensitivity Analysis (GSA) to explore numerically how our input parameters influence the risk. Our results confirm the important effects of pollen emission and loss. Most interestingly they highlight that the optimal spatial distribution of GM fields that mitigates the risk depends on our knowledge of the habitats of NTOs, and finally, moderate the influence of the dispersal kernel function. [ABSTRACT FROM AUTHOR]

Objectives: To quantify the energy expenditure of Australian Football training and matches and the total daily energy expenditure of Australian Football players using tri-axial accelerometers.Design: Cross sectional observation study.Methods: An algorithm was developed for the MiniMax 4.0 (Catapult Innovations, Scoresby Australia) using measured oxygen uptake and accelerometer data to estimate energy expenditure of 18 Australian Football players during training and matches. The algorithm was used to validate a metabolic power calculation used by Catapult Innovations (Scoresby Australia) in their proprietary GPS software. The SenseWear™ (Model MF-SW, Bodymedia, Pittsburgh, PA) armband was used to determine non-exercise activity thermogenesis and was worn for 7 days leading into a match. Training, match and non-exercise activity thermogenesis data was summed for total daily energy expenditure.Results: Energy expenditure for field training was estimated to be 2719±666kJ and for matches to be 5745±1468kJ. The estimated energy expenditure in the current study showed a large correlation (r=0.57, 90% CI 0.06-0.84) with the metabolic power calculation. The mean total daily energy expenditure for an in-season main training day was approximately 18,504kJ and match day approximately 19,160kJ with non-exercise activity thermogenesis contributing approximately 85% and 69% on training and match days, respectively.Conclusions: The MiniMax 4.0 and SenseWear™ armband accelerometers provide a practical, non-invasive and an effective method to successfully measure training and match energy expenditure, and non-exercise activity thermogenesis in field sport athletes. Taking methodological limitations into consideration, measuring energy expenditure allows for individualised nutrition programming to enhance performance and achieve body composition goals. [ABSTRACT FROM AUTHOR]

Abstract: A blended material composed of beta-tricalcium phosphate (β-TCP) and fumaric acid (FA) was prepared using a mechanochemical process. The structure and properties of the TCP–FA material was probed using particle size analysis, infrared, 31P and 13C solid-state nuclear magnetic resonance (NMR) spectroscopy, powder X-ray diffraction and calcium bioavailability. NMR studies showed that orthophosphate environments within β-TCP remain largely unaffected in the presence of FA during mechanochemical processing; alternately, 13C data indicated the carboxylic groups of FA are strongly affected during processing with β-TCP. X-ray results reveal β-TCP diffraction plane shifting with lattice contractions likely arising at the C 3 symmetry site. While milled β-TCP (mTCP) produces a higher flux of bioavailable calcium relative to native β-TCP, the mechanochemical conditioning of TCP–FA generates more than seven times the level of ionic calcium relative to mTCP. Collectively, the results from these studies indicate FA interfaces with calcium oxide polyhedra of the β-TCP hexagonal crystal lattice, especially with the underbonded CaO3 cluster manifested within the C 3 symmetry site of the β-TCP motif. An in vitro remineralization/demineralization pH cycling dental model was then used to assess the potential of the TCP–FA material in reversing early stage non-cavitated enamel lesions. Characterization of the remineralization via surface and longitudinal microhardness measurements demonstrated that the TCP–FA material provides statistically superior remineralization relative to milled and native β-TCP. [Copyright &y& Elsevier]

In diabetes, glucagon secretion from pancreatic α cells is dysregulated. The underlying mechanisms, and whether dysfunction occurs uniformly among cells, remain unclear. We examined α cells from human donors and mice using electrophysiological, transcriptomic, and computational approaches. Rising glucose suppresses α cell exocytosis by reducing P/Q-type Ca2+ channel activity, and this is disrupted in type 2 diabetes (T2D). Upon high-fat feeding of mice, α cells shift toward a "β cell-like" electrophysiological profile in concert with indications of impaired identity. In human α cells we identified links between cell membrane properties and cell surface signaling receptors, mitochondrial respiratory chain complex assembly, and cell maturation. Cell-type classification using machine learning of electrophysiology data demonstrated a heterogenous loss of "electrophysiologic identity" in α cells from donors with type 2 diabetes. Indeed, a subset of α cells with impaired exocytosis is defined by an enrichment in progenitor and lineage markers and upregulation of an immature transcriptomic phenotype, suggesting important links between α cell maturation state and dysfunction. [Display omitted] • Glucose suppresses α cell exocytosis by inhibiting P/Q-type Ca2+ currents • Patch-seq links maturation, respiration, and receptor expression to α cell function • Dysfunction of α cells associates with a "β cell-like" electrophysiological signature • Impaired exocytosis occurs in α cells enriched for lineage and immaturity markers In diabetes, glucagon secretion from pancreatic α cells is dysregulated. Dai et al. examined electrical and transcriptomic α cell phenotypes and found that dysfunction in type 2 diabetes is linked to cell maturation state and impaired α cell identity. Notably, a subset of α cells enriched for lineage markers appears uniquely susceptible to dysfunction. [ABSTRACT FROM AUTHOR]

A heterozygous missense mutation of the islet β cell-enriched MAFA transcription factor (p.Ser64Phe [S64F]) is found in patients with adult-onset β cell dysfunction (diabetes or insulinomatosis), with men more prone to diabetes than women. This mutation engenders increased stability to the unstable MAFA protein. Here, we develop a S64F MafA mouse model to determine how β cell function is affected and find sex-dependent phenotypes. Heterozygous mutant males (MafA S64F/+ ) display impaired glucose tolerance, while females are slightly hypoglycemic with improved blood glucose clearance. Only MafA S64F/+ males show transiently higher MafA protein levels preceding glucose intolerance and sex-dependent changes to genes involved in Ca2+ signaling, DNA damage, aging, and senescence. MAFAS64F production in male human β cells also accelerate cellular senescence and increase senescence-associated secretory proteins compared to cells expressing MAFAWT. These results implicate a conserved mechanism of accelerated islet aging and senescence in promoting diabetes in MAFAS64F carriers in a sex-biased manner. [Display omitted] • MafA S64F/+ mice show sex-dependent β cell dysfunction (diabetes or hypoglycemia) • MafA S64F/+ male and female mice show aberrant islet Ca2+ signaling • Only MafA S64F/+ males show markers of islet aging and senescence • MAFAS64F expression in male human EndoC-βH2 cells accelerates cellular senescence Walker et al. show that mice harboring the missense mutation of the pancreatic islet-enriched transcription factor MAFA (S64F MAFA) demonstrate sex-dependent β cell dysfunction, similar to findings in human carriers. Only male S64F MAFA β cells show accelerated senescence and β cell dysfunction toward hyperglycemia. [ABSTRACT FROM AUTHOR]

Myt Transcription Factors Prevent Stress-Response Gene Overactivation to Enable Postnatal Pancreatic Cell Proliferation, Function, and Survival (Developmental Cell 53, 390-405.e1-e10; May 18, 2020) As a result of an author oversight in the originally published version of this article, the name of author Appakalai N. Balamurugan was incorrectly written as "Balamurugan N. Appakalai." The authors apologize for the error and any inconvenience that may have resulted. [Extracted from the article]

Summary Islet β cells from newborn mammals exhibit high basal insulin secretion and poor glucose-stimulated insulin secretion (GSIS). Here we show that β cells of newborns secrete more insulin than adults in response to similar intracellular Ca 2+ concentrations, suggesting differences in the Ca 2+ sensitivity of insulin secretion. Synaptotagmin 4 (Syt4), a non-Ca 2+ binding paralog of the β cell Ca 2+ sensor Syt7, increased by ∼8-fold during β cell maturation. Syt4 ablation increased basal insulin secretion and compromised GSIS. Precocious Syt4 expression repressed basal insulin secretion but also impaired islet morphogenesis and GSIS. Syt4 was localized on insulin granules and Syt4 levels inversely related to the number of readily releasable vesicles. Thus, transcriptional regulation of Syt4 affects insulin secretion; Syt4 expression is regulated in part by Myt transcription factors, which repress Syt4 transcription. Finally, human SYT4 regulated GSIS in EndoC-βH1 cells, a human β cell line. These findings reveal the role that altered Ca 2+ sensing plays in regulating β cell maturation. [ABSTRACT FROM AUTHOR]

We applied a novel measure of average lifespan shortened (ALSS) to examine changes in lifespan among patients who died of cancer over a 10-year period from 2006 to 2016 in 20 selected high-income countries from North America, Europe, Asia, and Oceania. We retrieved cancer deaths in each country from the World Health Organization mortality database. We calculated ALSS as a ratio of years of life lost to the expected lifespan among patients who died from cancer. Between 2006 and 2016, we observed modest changes in ALSS for overall cancer deaths over the study in many countries. The changes in the ALSS over time due to any cancer ranged between -1.7 and +0.4 percentage points (pps) among men and between -1.9 and +0.6 pps among women. Across countries, overall cancer deaths led to an average loss between 16% and 22% of their lifespan in men, and between 18% and 24% in women. Across cancer sites, patients who died of central nervous system cancers, for instance, lost a large proportion of their lifespan. In this study, we demonstrated the use of ALSS across selected high-income countries, which enables population-level assessment of premature mortality among cancer patients over time. [ABSTRACT FROM AUTHOR]