Analysis of permanent magnets as elasmobranch bycatch reduction devices in hook-and-line and longline trials

Previous studies indicate that elasmobranch fishes (sharks, skates and rays) detect the Earth’s geomagnetic field by indirect magnetoreception through electromagnetic induction, using their ampullae of Lorenzini. Applying this concept, we evaluated the capture of elasmobranchs in the presence of permanent magnets in hook-and-line and inshore longline fishing experiments. Hooks with neodymium-iron-boron magnets significantly reduced the capture of elasmobranchs overall in comparison with control and procedural control hooks in the hook-and-line experiment. Catches of Atlantic sharpnose shark (Rhizoprionodon terraenovae) and smooth dogfish (Mustelus canis) were signif icantly reduced with magnetic hook-and-line treatments, whereas catches of spiny dogfish (Squalus acanthias) and clearnose skate (Raja eglanteria) were not. Longline hooks with barium-ferrite magnets significantly reduced total elasmobranch capture when compared with control hooks. In the longline study, capture of blacktip sharks (Carcharhinus limbatus) and southern stingrays (Dasyatis americana) was reduced on magnetic hooks, whereas capture of sandbar shark (Carcharhinus plumbeus) was not affected. Teleosts, such as red drum (Sciaenops ocellatus), Atlantic croaker (Micropogonias undulatus), oyster toadfish (Opsanus tau), black sea bass (Centropristis striata), and the bluefish (Pomatomas saltatrix), showed no hook preference in either hook-and-line or longline studies. These results indicate that permanent magnets, although eliciting species-specific capture trends, warrant further investigation in commercial longline and recreational fisheries, where bycatch mortality is a leading contributor to declines in elasmobranch populations

Noggin null allele mice exhibit a microform of holoprosencephaly

Holoprosencephaly (HPE) is a heterogeneous craniofacial and neural developmental anomaly characterized in its most severe form by the failure of the forebrain to divide. In humans, HPE is associated with disruption of Sonic hedgehog and Nodal signaling pathways, but the role of other signaling pathways has not yet been determined. In this study, we analyzed mice which, due to the lack of the Bmp antagonist Noggin, exhibit elevated Bmp signaling. Noggin−/− mice exhibited a solitary median maxillary incisor that developed from a single dental placode, early midfacial narrowing as well as abnormalities in the developing hyoid bone, pituitary gland and vomeronasal organ. In Noggin−/− mice, the expression domains of Shh, as well as the Shh target genes Ptch1 and Gli1, were reduced in the frontonasal region at key stages of early facial development. Using E10.5 facial cultures, we show that excessive BMP4 results in reduced Fgf8 and Ptch1 expression. These data suggest that increased Bmp signaling in Noggin−/− mice results in downregulation of the hedgehog pathway at a critical stage when the midline craniofacial structures are developing, which leads to a phenotype consistent with a microform of HP

The upper airway response to pollen is enhanced by exposure to combustion particulates: a pilot human experimental challenge study.

Although human experimental studies have shown that gaseous pollutants enhance the inflammatory response to allergens, human data on whether combustion particulates enhance the inflammatory response to allergen are limited. Therefore, we conducted a human experimental study to investigate whether combustion particulates enhance the inflammatory response to aeroallergens. "Enhancement" refers to a greater-than-additive response when combustion particulates are delivered with allergen, compared with the responses when particulates and allergen are delivered alone. Eight subjects, five atopic and three nonatopic, participated in three randomized exposure-challenge sessions at least 2 weeks apart (i.e., clean air followed by allergen, particles followed by no allergen, or particles followed by allergen). Each session consisted of nasal exposure to combustion particles (target concentration of 1.0 mg/m3) or clean air for 1 hr, followed 3 hr later by challenge with whole pollen grains or placebo. Nasal lavage was performed immediately before particle or clean air exposure, immediately after exposure, and 4, 18 and 42 hr after pollen challenge. Cell counts, differentials, and measurement of cytokines were performed on each nasal lavage. In atopic but not in nonatopic subjects, when allergen was preceded by particulates, there was a significant enhancement immediately after pollen challenge in nasal lavage leukocytes and neutrophils (29.7 X 10(3) cells/mL and 25.4 X 10(3) cells/mL, respectively). This represents a 143% and 130% enhancement, respectively. The enhanced response for interleukin-4 was 3.23 pg/mL (p = 0.06), a 395% enhancement. In atopic subjects there was evidence of an enhanced response when particulates, as compared to clean air, preceded the allergen challenge

The Upper Airway Response to Pollen is Enhanced by Exposure to Combustion Particulates: A Pilot Human Experimental Challenge Study.

Although human experimental studies have shown that gaseous pollutants enhance the inflammatory response to allergens, human data on whether combustion particulates enhance the inflammatory response to allergen are limited. Therefore, we conducted a human experimental study to investigate whether combustion particulates enhance the inflammatory response to aeroallergens. "Enhancement" refers to a greater-than-additive response when combustion particulates are delivered with allergen, compared with the responses when particulates and allergen are delivered alone. Eight subjects, five atopic and three nonatopic, participated in three randomized exposure-challenge sessions at least 2 weeks apart (i.e., clean air followed by allergen, particles followed by no allergen, or particles followed by allergen). Each session consisted of nasal exposure to combustion particles (target concentration of 1.0 mg/m$^3$) or clean air for 1 hr, followed 3 hr later by challenge with whole pollen grains or placebo. Nasal lavage was performed immediately before particle or clean air exposure, immediately after exposure, and 4, 18 and 42 hr after pollen challenge. Cell counts, differentials, and measurement of cytokines were performed on each nasal lavage. In atopic but not in nonatopic subjects, when allergen was preceded by particulates, there was a significant enhancement immediately after pollen challenge in nasal lavage leukocytes and neutrophils (29.7 X 10$^3$ cells/mL and 25.4 X 10$^3$ cells/mL, respectively). This represents a 143% and 130% enhancement, respectively. The enhanced response for interleukin-4 was 3.23 pg/mL (p = 0.06), a 395% enhancement. In atopic subjects there was evidence of an enhanced response when particulates, as compared to clean air, preceded the allergen challenge

Pervasive Genetic Hitchhiking and Clonal Interference in 40 Evolving Yeast Populations

The dynamics of adaptation determines which mutations fix in a population, and hence how reproducible evolution will be. This is central to understanding the spectra of mutations recovered in evolution of antibiotic resistance1, the response of pathogens to immune selection2,3, and the dynamics of cancer progression4,5. In laboratory evolution experiments, demonstrably beneficial mutations are found repeatedly6–8, but are often accompanied by other mutations with no obvious benefit. Here we use whole-genome whole-population sequencing to examine the dynamics of genome sequence evolution at high temporal resolution in 40 replicate Saccharomyces cerevisiae populations growing in rich medium for 1,000 generations. We find pervasive genetic hitchhiking: multiple mutations arise and move synchronously through the population as mutational “cohorts.” Multiple clonal cohorts are often present simultaneously, competing with each other in the same population. Our results show that patterns of sequence evolution are driven by a balance between these chance effects of hitchhiking and interference, which increase stochastic variation in evolutionary outcomes, and the deterministic action of selection on individual mutations, which favors parallel evolutionary solutions in replicate populations

Energetics of hydrogen impurities in aluminum and their effect on mechanical properties

The effects of hydrogen impurities in the bulk and on the surface of aluminum are theoretically investigated. Within the framework of density functional theory, we have obtained the dependence on H concentration of the stacking fault energy, the cleavage energy, the Al/H surface energy and the Al/H/Al interface formation energy. The results indicate a strong dependence of the slip energy barrier in the $[\bar 211]$ direction the cleavage energy in the [111] direction and the Al/H/Al interface formation energy, on H concentration and on tension. The dependence of the Al/H surface energy on H coverage is less pronounced, while the optimal H coverage is $\leq 0.25$ monolayer. The calculated activation energy for diffusion between high symmetry sites in the bulk and on the surface is practically the same, 0.167 eV. From these results, we draw conclusions about the possible effect of H impurities on mechanical properties, and in particular on their role in embrittlement of Al.Comment: 9 pages, 5 figure

A genomic and evolutionary approach reveals non-genetic drug resistance in malaria

Background: Drug resistance remains a major public health challenge for malaria treatment and eradication. Individual loci associated with drug resistance to many antimalarials have been identified, but their epistasis with other resistance mechanisms has not yet been elucidated. Results: We previously described two mutations in the cytoplasmic prolyl-tRNA synthetase (cPRS) gene that confer resistance to halofuginone. We describe here the evolutionary trajectory of halofuginone resistance of two independent drug resistance selections in Plasmodium falciparum. Using this novel methodology, we discover an unexpected non-genetic drug resistance mechanism that P. falciparum utilizes before genetic modification of the cPRS. P. falciparum first upregulates its proline amino acid homeostasis in response to halofuginone pressure. We show that this non-genetic adaptation to halofuginone is not likely mediated by differential RNA expression and precedes mutation or amplification of the cPRS gene. By tracking the evolution of the two drug resistance selections with whole genome sequencing, we further demonstrate that the cPRS locus accounts for the majority of genetic adaptation to halofuginone in P. falciparum. We further validate that copy-number variations at the cPRS locus also contribute to halofuginone resistance. Conclusions: We provide a three-step model for multi-locus evolution of halofuginone drug resistance in P. falciparum. Informed by genomic approaches, our results provide the first comprehensive view of the evolutionary trajectory malaria parasites take to achieve drug resistance. Our understanding of the multiple genetic and non-genetic mechanisms of drug resistance informs how we will design and pair future anti-malarials for clinical use. Electronic supplementary material The online version of this article (doi:10.1186/s13059-014-0511-2) contains supplementary material, which is available to authorized users