Genetic variation in transferrin as a predictor for differentiation and evolution of caribou from eastern Canada

Polycrylamide gel electrophoresis was used to analyse tranferrrin variation in caribou populations from Manitoba, Ontario, Québec/Labrador, and from Baffin Island, Northwest Territories in eastern Canada. The transferrin allele frequencies in these populations were compared with those previously reported for Canadian barren-ground caribou, Rangifer tarandus groenlandicus, Alaska caribou, R.t. grand, Peary caribou, R.t. pearyi, Svalbard reindeer, R.t. pla-tyrhynchus, and Eurasian tundra reindeer, R.t. tarandus. A total of twenty different alleles was detected in the analysed material, considerable genetic heterogeneity being detected among regions. Three alleles that were relatively common in caribou from Ontario, Manitoba and Québec/Labrador, were not present in R.t. grand, R.t. pearyi, R.t. tarandus or R.t. platyrhynchus, and present only at very low frequencies 'm R.t. groenlandicus. These findings, together with genetic identity analyses, suggest that the caribou in Manitoba, Ontario, and Québec/Labrador are mainly of the R.t. caribou type, and that little interbreeding has occurred with other subspecies. The large genetic distance in the transferrin locus between R.t. caribou and other subspecies of reindeer/caribou suggests that, during the Wisconsin glaciation the ancestral populations of R.t. caribou survived in a refugium different from that of the ancestral populations of the other subspecies. Significant genetic differences between Baffin Island caribou and all other populations were mainly due to the presence of one allele that was in high frequency in Baffin Island caribou, but that was absent, or present in very low frequencies, in all other reindeer/caribou populations. The genetic differences between Baffin Island caribou and the other subspecies were greater than the differences between several of the currently recognized subspecies

Direct measurement of the flow field around swimming microorganisms

Swimming microorganisms create flows that influence their mutual interactions and modify the rheology of their suspensions. While extensively studied theoretically, these flows have not been measured in detail around any freely-swimming microorganism. We report such measurements for the microphytes Volvox carteri and Chlamydomonas reinhardtii. The minute ~0.3% density excess of V. carteri over water leads to a strongly dominant Stokeslet contribution, with the widely-assumed stresslet flow only a correction to the subleading source dipole term. This implies that suspensions of V. carteri have features similar to suspensions of sedimenting particles. The flow in the region around C. reinhardtii where significant hydrodynamic interaction is likely to occur differs qualitatively from a "puller" stresslet, and can be described by a simple three-Stokeslet model.Comment: 4 pages, 4 figures, accepted for publication in PR

Study of filamentation with a high power high repetition rate ps laser at 1.03 µm

International audienceWe study the propagation of intense, high repetition rate laser pulses of picosecond duration at 1.03 µm central wavelength through air. Evidence of filamentation is obtained from measurements of the beam profile as a function of distance, from photoemission imaging and from spatially resolved sonometric recordings. Good agreement is found with numerical simulations. Simulations reveal an important self shortening of the pulse duration, suggesting that laser pulses with few optical cycles could be obtained via double filamentation. An important lowering of the voltage required to induce guided electric discharges between charged electrodes is measured at high laser pulse repetition rate.-repetition-rate picosecond pump laser based on a Yb:YAG disk amplifier for optical parametric amplification

Stabilizing Soybean Production in Northeast Texas with Early Planting of Early-Maturing Soybean Varieties.

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Practice makes the model: a critical review of stormwater green infrastructure modelling practice

Green infrastructures (GIs) have in recent decades emerged as sustainable technologies for urban stormwater management, and numerous studies have been conducted to develop and improve hydrological models for GIs. This review aims to assess current practice in GI hydrological modelling, encompassing the selection of model structure, equations, model parametrization and testing, uncertainty analysis, sensitivity analysis, the selection of objective functions for model calibration, and the interpretation of modelling results. During a quantitative and qualitative analysis, based on a paper analysis methodology applied across a sample of 270 published studies, we found that the authors of GI modelling studies generally fail to justify their modelling choices and their alignments between modelling objectives and methods. Some practices, such as uncertainty analysis, were also found to be limited, despite their necessity being widely acknowledged by the scientific community and their application in other fields. In order to improve current GI modelling practice, the authors suggest the following: i) a framework, called STAMP, designed to promote the standardisation of the documentation of GI modelling studies, and ii) improvements in modelling tools for facilitating good practices, iii) the sharing of data for better model testing, iv) the evaluation of the suitability of hydrological equations for GI application, v) the publication of clear statements regarding model limitations and negative results.publishedVersio

The CHeriScape project, 2014-2016 : key messages from CHeriScape : cultural solutions for cultural problems

publishedVersio

Clinical impact and proposed application of molecular markers, genetic variants, and cytogenetic analysis in mast cell neoplasms: Status 2022

Mast cell neoplasms are an emerging challenge in the fields of internal medicine, allergy, immunology, dermatology, laboratory medicine, and pathology. In this review, we discuss the current standards for the diagnosis and prognostication of mast cell neoplasms with special reference to clinically relevant germline and somatic gene variants. In patients with cutaneous mastocytosis or with indolent systemic mastocytosis (SM), various KIT-activating mutations act as key molecular drivers of the disease. In adults, KIT p.D816V is by far the most prevalent driver, whereas other KIT mutants are detected in nearly 40% of children. In advanced SM, including aggressive SM, SM with an associated hematological neoplasm, and mast cell leukemia, additional somatic mutations in other genes, such as SRSF2, JAK2, RUNX1, ASXL1, or RAS, may be detected. These drivers are more frequently detected in SM with an associated hematological neoplasm, particularly in male patients. Recently, hereditary alpha-tryptasemia has been identified as a genetic trait more prevalent in SM compared with healthy controls. Moreover, hereditary alpha-tryptasemia is more frequent in patients with SM with Hymenoptera venom allergy and severe mediator-related symptoms than in patients with SM without symptoms. On the basis of this knowledge, we propose a diagnostic algorithm in which genetic markers are applied together with clinical and histopathologic criteria to establish the diagnosis and prognosis in SM

Standards of genetic testing in the diagnosis and prognostication of systemic mastocytosis in 2022: Recommendations of the EU-US cooperative group

Mastocytosis comprises rare heterogeneous diseases characterized by an increased accumulation of abnormal mast cells in various organs/tissues. The pathogenesis of mastocytosis is strongly linked to the presence of KIT-activating mutations. In systemic mastocytosis (SM), the most frequent mutation encountered is KIT p.D816V, whose presence constitutes one of the minor diagnostic criteria. Different techniques are used to search and quantify the KIT p.D816V mutant; however, allele-specific quantitative PCR and droplet digital PCR are today the most sensitive. The analysis of the KIT p.D816V allele burden has undeniable interest for diagnostic, prognostic, and therapeutic monitoring. The analysis of non–mast cell hematological compartments in SM is similarly important because KIT p.D816V multilineage involvement is associated with a worse prognosis. In addition, in advanced forms of SM, mutations in genes other than KIT are frequently identified and affect negatively disease outcome and response to therapy. Thus, combined quantitative and sensitive analysis of KIT mutations and next-generation sequencing of other recurrently involved myeloid genes make it possible to better characterize the extent of the affected cellular compartments and additional molecular aberrations, providing a more detailed overview of the complex mutational landscape of SM, in relation with the clinical heterogeneity of the disease. In this article, we report the latest recommendations of the EU-US Cooperative Group presented in September 2020 in Vienna during an international working conference, on the techniques we consider standard to detect and quantify the KIT p.D816V mutant in SM and additional myeloid mutations found in SM subtypes.D.D.M., J.J.L., and M.C.C. were supported by the Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health. P.V. was supported by the Austrian Science Fund (FWF) (grant nos. F4704-B20 and P32470-B)

Priming of microglia in a DNA-repair deficient model of accelerated aging

AbstractAging is associated with reduced function, degenerative changes, and increased neuroinflammation of the central nervous system (CNS). Increasing evidence suggests that changes in microglia cells contribute to the age-related deterioration of the CNS. The most prominent age-related change of microglia is enhanced sensitivity to inflammatory stimuli, referred to as priming. It is unclear if priming is due to intrinsic microglia ageing or induced by the ageing neural environment. We have studied this in Ercc1 mutant mice, a DNA repair-deficient mouse model that displays features of accelerated aging in multiple tissues including the CNS. In Ercc1 mutant mice, microglia showed hallmark features of priming such as an exaggerated response to peripheral lipopolysaccharide exposure in terms of cytokine expression and phagocytosis. Specific targeting of the Ercc1 deletion to forebrain neurons resulted in a progressive priming response in microglia exemplified by phenotypic alterations. Summarizing, these data show that neuronal genotoxic stress is sufficient to switch microglia from a resting to a primed state

Mast cells as a unique hematopoietic lineage and cell system:From Paul Ehrlich's visions to precision medicine concepts

The origin and functions of mast cells (MCs) have been debated since their description by Paul Ehrlich in 1879. MCs have long been considered 'reactive bystanders' and 'amplifiers' in inflammatory processes, allergic reactions, and host responses to infectious diseases. However, knowledge about the origin, phenotypes and functions of MCs has increased substantially over the past 50 years. MCs are now known to be derived from multipotent hematopoietic progenitors, which, through a process of differentiation and maturation, form a unique hematopoietic lineage residing in multiple organs. In particular, MCs are distinguishable from basophils and other hematopoietic cells by their unique phenotype, origin(s), and spectrum of functions, both in innate and adaptive immune responses and in other settings. The concept of a unique MC lineage is further supported by the development of a distinct group of neoplasms, collectively referred to as mastocytosis, in which MC precursors expand as clonal cells. The clinical consequences of the expansion and/or activation of MCs are best established in mastocytosis and in allergic inflammation. However, MCs have also been implicated as important participants in a number of additional pathologic conditions and physiological processes. In this article, we review concepts regarding MC development, factors controlling MC expansion and activation, and some of the fundamental roles MCs may play in both health and disease. We also discuss new concepts for suppressing MC expansion and/or activation using molecularly-targeted drugs