Discovery of two bright DO-type white dwarfs

We discovered two bright DO-type white dwarfs, GALEXJ053628.3+544854 (J0536+5448) and GALEX231128.0+292935(J2311+2929), which rank among the eight brightest DO-type white dwarfs known. Our non-LTE model atmosphere analysis reveals effective temperatures and surface gravities of $T_{\mathrm{eff}}=80000\pm4600\,\mathrm{K}$ and $\log \mathrm{g}=8.25\pm0.15$ for J0536+5448 and $T_{\mathrm{eff}}=69400\pm900\,\mathrm{K}$ and $\log \mathrm{g}=7.80\pm0.06$ for J2311+2929. The latter shows a significant amount of carbon in its atmosphere ($C=0.003^{+0.005}_{-0.002}$, by mass), while for J0536+5448 we could derive only an upper limit of $C<0.003$. Furthermore, we calculated spectroscopic distances for the two stars and found a good agreement with the distances derived from the Gaia parallaxes.Comment: 7 pages, 4 figures, accepted for publication in MNRA

Review: Eric A. Posner and David Weisbach: Climate Change Justice

Book Review Eric A. Posner and David Weisbach (2010): Climate Change Justice. Princeton: Princeton University Press. 220 pages. ISBN: 978-0- 691-13775-9. Price $27.95

Regulation of Zebrafish Hindbrain Development by Fibroblast Growth Factor and Retinoic Acid: A Dissertation

Fibroblast growth factor (Fgf) and Retinoic acid (RA) are known to be involved in patterning the posterior embryo. Work has shown that Fgf can convert anterior tissue into posterior fates and that embryos deficient in Fgf signaling lack posterior trunk and tail structures. Likewise, studies performed on RA have shown that overexpression of RA posteriorizes anterior tissue, while disrupting RA signaling yields a loss of posterior fates. While it appears these signals are necessary for posterior development, the role Fgf and RA play in development of the hindbrain is still enigmatic. A detailed study of the requirements for Fgf and RA in the early vertebrate hindbrain are lacking, namely due to a deficiency in gene markers for the presumptive hindbrain at early developmental stages. In this study, we make use of recently isolated genes, which are expressed in the presumptive hindbrain region at early developmental stages, to explore Fgf and RA regulation of the early vertebrate hindprain. We employed both overexpression and loss of function approaches to explore the role of Fgf in early vertebrate development with an emphasis on the presumptive hindbrain region in zebrafish embryos. By loss of function analysis, we show that Fgf regulates genes expressed exclusively in the hindbrain region (meis3 and hoxbla) as well as genes whose expression domains encompass both the hindbrain and more caudal regions (nlz and hoxb1b), thus demonstrating a requirement for Fgf signaling throughout the anteroposterior axis of the hindbrain (rostral to caudal hindbrain) by mid-gastrula stages. To further characterize early gene regulation by Fgf, we utilized an in vitro system and found that Fgf is sufficient to induce nlz directly and hoxb1b indirectly, while it does not induce meis3 or hoxb1a. Furthermore, in vivo work demonstrates that Fgf soaked beads can induce nlz and hoxb1b adjacent to the bead and meis3at a distance. Given the regulation of these genes in vitro and in vivo by Fgf and their position along the rostrocaudal axis of the embryo, our results suggest an early acting Fgf resides in the caudal end of the embryo and signals at a distance to the hindbrain. We detect a similar regulation of hindbrain genes by RA at gastrula stages as well, suggesting that both factors are essential for early hindbrain development. Interestingly however, we find that the relationship between Fgf and RA is dynamic throughout development. Both signals are required at gastrula stages as disruption of either pathway alone disrupts hindbrain gene expression, but a simultaneous disruption of both pathways at later stages is required to disrupt the hindbrain. We suggest that Fgf and RA are present in limiting concentrations at gastrula stages, such that both factors are required for gene expression or that one factor is necessary for activation of the other. Our results also reveal a changing and dynamic relationship between Fgf and RA in the regulation of the zebrafish hindbrain, suggesting that at segmentation stages, Fgf and RA may no longer be limiting or that they are no longer interdependent. As we have demonstrated that an early Fgf signal is required for gastrula stage hindbrain development, we next questioned which Fgf performed this function. We have demonstrated that the early Fgf signal required for hindbrain development is not Fgf3 or Fgf8, two Fgfs known to be involved in signaling centers at the mid-hindbrain boundary (MHB) and rhombomere (r) 4. We further show that two recently identified Fgfs, Fgf4 and Fgf24 are also insufficient alone or in combination with other known Fgfs to regulate hindbrain gene expression. However, as Fgfs may act combinatorially, we do not rule out the possibility of their involvement in early hindbrain gene regulation. However, as time passes and additional Fgfs are isolated and cloned, the elusive Fgf signal required for early hindbrain development will likely be identified. Taken together, we propose that an early acting Fgf residing in the caudal end of the embryo regulates hindbrain genes together with RA at gastrula stages. We suggest that both Fgf and RA are required for gene expression at gastrula stages, but this requirements changes over time as Fgf and RA become redundant. We also demonstrate that the Fgf required for gastrula stage hindbrain development has yet to be identified

Regulation of Zebrafish Hindbrain Development by Fibroblast Growth Factor and Retinoic Acid: A Dissertation

A thesis submitted to the Department of Biochemistry and Molecular Pharmacology and the Graduate School of Biomedical Sciences of the University of Massachusetts, Worcester in partial fulfilment of the requirements for the degree of Doctor of Philosophy, Biochemistry and Molecular Pharmacology. Fibroblast growth factor (Fgf) and Retinoic acid (RA) are known to be involved in patterning the posterior embryo. Work has shown that Fgf can convert anterior tissue into posterior fates and that embryos deficient in Fgf signaling lack posterior trunk and tail structures. Likewise, studies performed on RA have shown that overexpression of RA posteriorizes anterior tissue, while disrupting RA signaling yields a loss of posterior fates. While it appears these signals are necessary for posterior development, the role Fgf and RA play in development of the hindbrain is still enigmatic. A detailed study of the requirements for Fgf and RA in the early vertebrate hindbrain are lacking, namely due to a deficiency in gene markers for the presumptive hindbrain at early developmental stages. In this study, we make use of recently isolated genes, which are expressed in the presumptive hindbrain region at early developmental stages, to explore Fgf and RA regulation of the early vertebrate hindbrain

Michigan Production Costs for Tart Cherries by Production Region

The weighted average cost of producing tart cherries in Michigan on a representative farm in 2009 is $0.36/lb. This cost was averaged across the three main production regions in Michigan and weighted by average per acre production for each region as published by the Michigan Agricultural Statistics Service. --Costs vary across the main production regions and by farm size. Costs are about$0.04/lb less for mid-sized farms in Northwest Michigan and $0.08/lb and$0.10/lb in West Central and Southwest Michigan, respectively. --This report was developed through interviews with tart cherry growers and other experts in each of the three main growing regions in 2005 and 2006. Many of the numbers were updated in 2009. --The cost of production calculation is based on estimates of operating costs, harvest costs, and management, interest and tax costs. It also includes an amortized cost of establishing an orchard and employing the land in production (versus some other use). The following tables summarize the cost findings for each of the production regions.Tart cherry, costs, production, Michigan, Agribusiness, Crop Production/Industries, Q100, Q120,

Butyl Benzyl Phthalate (BBP) Induces Caudal Defects During Embryonic Development

Butyl benzyl phthalate (BBP) is commonly added during the manufacturing of plastics to increase flexibility and elasticity. However, BBP leaches off of plastic and environment presence has been detected in soil, groundwater and sediment potentially effecting organisms in the environment. Given the widespread uses of BBP in household, consumer goods and the presence of BBP in the environment, studies on developmental toxicity are needed. Here, we use a zebrafish model to investigate the early developmental toxicity of BBP. We treated gastrula staged embryos with increasing concentrations of BBP and noted concentration-dependent defects in caudal tail development, but the effect was caudal specific with no other developmental defects noted. In situ hybridization studies using muscle and notochord markers show alterations in muscle development and non-linear, kinked notochord staining. A more detailed antibody staining using a myosin specific marker shows disorganized myofibrils and a loss of chevron shaped somites. Furthermore, vascular development in the tail was also disrupted in a concentration dependent manner. We conclude that BBP is toxic to caudal development in zebrafish. The sensitivity of zebrafish during development to environmental toxins and chemicals has been useful in assessing the health of the aquatic environment. The results presented here are a useful early warning system for contamination that could affect human health

Glyphosate Induces Neurotoxicity in Zebrafish

Glyphosate based herbicides (GBH) like Roundup® are used extensively in agriculture as well as in urban and rural settings as a broad spectrum herbicide. Its mechanism of action was thought to be specific only to plants and thus considered safe and non-toxic. However, mounting evidence suggests that GBHs may not be as safe as once thought as initial studies in frogs suggest that GBHs may be teratogenic. Here we utilize the zebrafish vertebrate model system to study early effects of glyphosate exposure using technical grade glyphosate and the Roundup® Classic formulation. We find morphological abnormalities including cephalic and eye reductions and a loss of delineated brain ventricles. Concomitant with structural changes in the developing brain, using in situ hybridization analysis, we detect decreases in genes expressed in the eye, fore and midbrain regions of the brain including pax2, pax6, otx2 and ephA4. However, we do not detect changes in hindbrain expression domains of ephA4 nor exclusive hindbrain markers krox-20 and hoxb1a. Additionally, using a Retinoic Acid (RA) mediated reporter transgenic, we detect no alterations in the RA expression domains in the hindbrain and spinal cord, but do detect a loss of expression in the retina. We conclude that glyphosate and the Roundup® formulation is developmentally toxic to the forebrain and midbrain but does not affect the hindbrain after 24 hour exposure