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The article examines the genealogy of Mary (Browne) (Oakley) Bouchier alias Garret of Saffron Walden, Essex, England and Massachusetts and her family, dealing with topics including the Great Migration Study Project, birth records, and parish registers.

The recovery of a cache of lithic bifaces (the Bouchier Cache) is reported from an ecotonal area located between the southern High Plains (Llano Estacado) and Central Lowlands (western Rolling Plains). The homogenous nature of the bifacial cores suggests that the cache represents a resource stockpile, and, therefore, is important to understanding hunter-gatherer logistical mobility strategies on the southern Plains. Bifacial core caches are a distinctly recognizable component of caching behavior that do not appear to be restricted to particular cultural groups, time periods, or geographic locations. The age and cultural association of this cache is not known. Morphological and technological examination suggests the cache would fit well with models of high residential mobility typically attributed to early and middle Holocene populations.

Summarizes topics discussed by Doctor Diane Bouchier, founder of the American Society of Botanical Artists (ASBA) in the 2004 annual meeting of ASBA in the U.S. Background on the foundation of the ASBA; Challenges faced by founders in establishing the botanical artists' organization; Factors that contributed to the success of the society; List of botanical artists acknowledged by Bouchier for contributions in the society.

The article offers information on Bouchier Group, a company which provides civil construction and on-site services in Alberta. Topics include the views of Nicole Bourque-Bouchier, owner of the company, on the requirement of an entrepreneurial spirit in entrepreneurship, the addition of railroad maintenance business and security services to the company and the partnership of Bouchier with construction services firm Carillion Plc, as of May 2014.

The article announces that botanical artist John Pastoriza-Piñol has been presented the 2013 Diane Bouchier Artist Award for Excellence in Botanical Art.

Background: Dairy cattle breeds are populations of limited effective size, subject to recurrent outbreaks of recessive defects that are commonly studied using positional cloning. However, this strategy, based on the observation of animals with characteristic features, may overlook a number of conditions, such as immune or metabolic genetic disorders, which may be confused with pathologies of environmental etiology. Results: We present a data mining framework specifically designed to detect recessive defects in livestock that have been previously missed due to a lack of specific signs, incomplete penetrance, or incomplete linkage disequilibrium. This approach leverages the massive data generated by genomic selection. Its basic principle is to compare the observed and expected numbers of homozygotes for sliding haplotypes in animals with different life histories. Within three cattle breeds, we report 33 new loci responsible for increased risk of juvenile mortality and present a series of validations based on large-scale genotyping, clinical examination, and functional studies for candidate variants affecting the NOA1, RFC5, and ITGB7genes. In particular, we describe disorders associated with NOA1and RFC5mutations for the first time in vertebrates. Conclusions: The discovery of these many new defects will help to characterize the genetic basis of inbreeding depression, while their management will improve animal welfare and reduce losses to the industry.

Focuses on the professional life of Diane Bouchier as a botanical artist form Stony Brook, New York. Career Background; Skills; Accomplishments.

In addition to its classical role in apoptosis, accumulating evidence suggests that caspase-2 has non-apoptotic functions, including regulation of cell division. Loss of caspase-2 is known to increase proliferation rates but how caspase-2 is regulating this process is currently unclear. We show that caspase-2 is activated in dividing cells in G1-phase of the cell cycle. In the absence of caspase-2, cells exhibit numerous S-phase defects including delayed exit from S-phase, defects in repair of chromosomal aberrations during S-phase, and increased DNA damage following S-phase arrest. In addition, caspase-2-deficient cells have a higher frequency of stalled replication forks, decreased DNA fiber length, and impeded progression of DNA replication tracts. This indicates that caspase-2 protects from replication stress and promotes replication fork protection to maintain genomic stability. These functions are independent of the pro-apoptotic function of caspase-2 because blocking caspase-2-induced cell death had no effect on cell division, DNA damage-induced cell cycle arrest, or DNA damage. Thus, our data supports a model where caspase-2 regulates cell cycle and DNA repair events to protect from the accumulation of DNA damage independently of its pro-apoptotic function.

L’ischémie cérébrale retardée (ICR) reste une complication fréquente et dramatique de l’hémorragie méningée anévrismale, dont l’incidence, élevée avant le onzième jour post-saignement, impose une surveillance continue. Le diagnostic clinique d’une anomalie de perfusion avec un déficit neurologique peut être rendu difficile chez les patients qui ont des troubles de la conscience. La surveillance clinique seule est à risque de diagnostic trop tardif pour une prévention efficace de la lésion cérébrale définitive. Une approche multimodale pour un diagnostic précoce du risque d’ICR peut associer le Doppler transcrânien, de l’électrophysiologie, de l’oxymétrie ou du métabolisme cérébral, ou encore un biomarqueur plasmatique, qui devra être confirmé par une imagerie de perfusion. Cette difficulté diagnostique reflète la complexité des mécanismes à l’origine de l’ICR que les études expérimentales ont bien mis en évidence. En accord avec cette complexité, différentes stratégies de prévention thérapeutique ont ciblé la spasticité vasculaire, l’inflammation, l’agrégation plaquettaire, le métabolisme cérébral, ou l’élimination du sang dans les espaces sous-arachnoïdiens. Les résultats inconstants des études cliniques ont confirmé la complexité de la lésion d’ICR. La nimodipine reste le seul traitement préventif recommandé avec un impact sur le devenir neurologique. Plus récemment, l’antagoniste du récepteur à l’endothéline semblait efficace sur la vasomotricité des artères cérébrales sans amélioration du devenir neurologique. Les prochaines études cliniques devraient préciser l’intérêt des inhibiteurs des phosphodiestérases ou du drainage du liquide céphalorachidien. Là encore, une approche multimodale des thérapeutiques devrait permettre la prévention optimale de cette complication redoutable.

Yemen is currently experiencing, to our knowledge, the largest cholera epidemic in recent history. The first cases were declared in September 2016, and over 1.1 million cases and 2,300 deaths have since been reported1. Here we investigate the phylogenetic relationships, pathogenesis and determinants of antimicrobial resistance by sequencing the genomes of Vibrio choleraeisolates from the epidemic in Yemen and recent isolates from neighbouring regions. These 116 genomic sequences were placed within the phylogenetic context of a global collection of 1,087 isolates of the seventh pandemic V. choleraeserogroups O1 and O139 biotype El Tor2–4. We show that the isolates from Yemen that were collected during the two epidemiological waves of the epidemic1—the first between 28 September 2016 and 23 April 2017 (25,839 suspected cases) and the second beginning on 24 April 2017 (more than 1 million suspected cases)—are V. choleraeserotype Ogawa isolates from a single sublineage of the seventh pandemic V. choleraeO1 El Tor (7PET) lineage. Using genomic approaches, we link the epidemic in Yemen to global radiations of pandemic V. choleraeand show that this sublineage originated from South Asia and that it caused outbreaks in East Africa before appearing in Yemen. Furthermore, we show that the isolates from Yemen are susceptible to several antibiotics that are commonly used to treat cholera and to polymyxin B, resistance to which is used as a marker of the El Tor biotype.

Background: Sickle cell disease (SCD) is an inherited red blood cell disorder that impacts millions of people worldwide. Patients with SCD experience chronic hemolysis and have elevated serum levels of free heme. Free heme activates a variety of inflammatory pathways that contribute to the serious clinical complications of SCD. One of the inflammatory pathways activated by heme is the inflammatory caspase pathway. Our lab previously showed that heme exposure in macrophages leads to the activation of inflammatory caspase proteins caspase-1 and caspase-4. Activation of these proteins by heme leads to IL-1β release and pyroptosis, a form of inflammatory cell death. Patients with SCD have increased circulating IL-1β levels, indicating this pathway is active in patients. In mouse models, inflammatory caspases are required for hemolysis-induced neutrophil recruitment and lethality, indicating these proteins are central to hemolysis-induced inflammation. Despite the key role these proteins play following hemolysis, it remains unknown how heme activates inflammatory caspases. Interestingly, both caspase-1 and caspase-4 are required for heme-induced IL-1β release while caspase-4 alone is required for heme-induced pyroptosis. In fact, pyroptosis likely is required for IL-1β release from the cell. Based on this data, we hypothesized that caspase-4 is the apical step in this pathway and a key druggable target for controlling unchecked inflammation in SCD.

Caspase-2, one of the most evolutionarily conserved of the caspase family, has been implicated in maintenance of chromosomal stability and tumour suppression. Caspase-2 deficient (Casp2−/−) mice develop normally but show premature ageing-related traits and when challenged by certain stressors, succumb to enhanced tumour development and aneuploidy. To test how caspase-2 protects against chromosomal instability, we utilized an ex vivo system for aneuploidy where primary splenocytes from Casp2−/−mice were exposed to anti-mitotic drugs and followed up by live cell imaging. Our data show that caspase-2 is required for deleting mitotically aberrant cells. Acute silencing of caspase-2 in cultured human cells recapitulated these results. We further generated Casp2C320Smutant mice to demonstrate that caspase-2 catalytic activity is essential for its function in limiting aneuploidy. Our results provide direct evidence that the apoptotic activity of caspase-2 is necessary for deleting cells with mitotic aberrations to limit aneuploidy.

The kinetic formation of self-assembled Ge/Si hut clusters grown by ultra-high vacuum chemical-vapour deposition has been investigated by means of reflection high-energy electron diffraction, atomic force microscopy and photoluminescence spectroscopy. We show that point defects that are induced in the epilayers grown at substrate temperatures below 525 °C greatly influence the optical properties of Ge/Si hut clusters. We have investigated two approaches of sample annealing in order to remove point defects while minimizing Ge/Si intermixing: a long annealing at the growth temperature and a rapid annealing up to a temperature of 900 °C for a very short period of time. The obtained results appear to indicate that the long annealing at the growth temperature allows reducing the contribution of point defects, giving rise to the observation of the proper photoluminescence of the Ge/Si hut clusters. However, the long annealing could not completely remove point defects. A well-controlled rapid thermal annealing for a very short period of time is shown, on the other hand, to be efficient for removing point defects and minimize the Ge/Si intermixing. Our experiments illustrate a correlation between the increase of Ge/Si intermixing and the evolution of the optical properties from a quantum-dot to a quantum-well behaviour.

Both x-ray reflectometry and high-resolution x-ray diffractometry techniques are used for the assessment of individual layer thicknesses and interfacial profiles inside complicated heterostructures, such as semi-conductor multilayers. In particular, the use of Fourier transform-based numerical treatments applied to both the reflectivity curves and the high-resolution diffraction profiles allows a fast and precise determination of the individual layer thicknesses. Moreover, we show the potentiality of this method by reporting x-ray reflectometry and diffractometry studies on waveguides structures and superlattices. Typical layer thicknesses from 0.5 nm to more than 1 μm are accessible with these methods. We show the complementarity of both x-ray reflectometry and high-resolution diffraction techniques. Finally, the reliability of using a simulation software for the assessment of complicated interfacial roughness, such as segregation profiles, is reported. Key wordx-ray reflectometry, high-resolution x-ray diffractometry, semi-conductor heterostructures, thickness determination, Fourier Transform, interfacial segregation profiles.

ABSTRACTBypass of the d,d-transpeptidase activity of penicillin-binding proteins by an l,d-transpeptidase (Ldtfm) results in resistance to ampicillin and glycopeptides in Enterococcus faeciumM9, a mutant obtained by nine consecutive selection steps. Resistance requires activation of a cryptic locus for production of the essential tetrapeptide-containing substrate of Ldtfmand impaired activity of protein phosphatase StpA. Here, whole-genome sequencing revealed a high mutation rate for the entire selection procedure (79 mutations in 900 generations). Acquisition of a mutation in the mismatch repair gene mutLhad little impact on the frequency of rifampin-resistant mutants although the mutation spectrum of M9 was typical of impaired MutL with high transversion to transition (40/11) and substitution to deletion (51/28) ratios. M9 did not mainly accumulate neutral mutations since base substitutions occurred more frequently in coding sequences than expected (χ2= 5.0; P< 0.05) and silent mutations were underrepresented (χ2= 5.72; P< 0.02). None of the mutations directly affected recognition of the tetrapeptide substrate of Ldtfmby peptidoglycan synthesis enzymes. Instead, mutations appear to remodel regulatory circuits involving two-component regulatory systems and sugar metabolism. The high number of mutations required for activation of the l,d-transpeptidase pathway may strongly limit emergence of cross-resistance to ampicillin and glycopeptides by this mechanism.