D→K,lνD \rightarrow K, l \nu Semileptonic Decay Scalar Form Factor and ∣Vcs∣|V_{cs}| from Lattice QCD

We present a new study of D semileptonic decays on the lattice which employs the Highly Improved Staggered Quark (HISQ) action for both the charm and the light valence quarks. We work with MILC unquenched $N_f = 2 + 1$ lattices and determine the scalar form factor $f_0(q^2)$ for $D \rightarrow K, l \nu$ semileptonic decays. The form factor is obtained from a scalar current matrix element that does not require any operator matching. We develop a new approach to carrying out chiral/continuum extrapolations of $f_0(q^2)$. The method uses the kinematic "$z$" variable instead of $q^2$ or the kaon energy $E_K$ and is applicable over the entire physical $q^2$ range. We find $f^{D \rightarrow K}_0(0) \equiv f^{D \rightarrow K}_+(0) = 0.747(19)$ in the chiral plus continuum limit and hereby improve the theory error on this quantity by a factor of $\sim$4 compared to previous lattice determinations. Combining the new theory result with recent experimental measurements of the product $f^{D \rightarrow K}_+(0) * |V_{cs}|$ from BaBar and CLEO-c leads to the most precise direct determination of the CKM matrix element $|V_{cs}|$ to date, $|V_{cs}| = 0.961(11)(24)$, where the first error comes from experiment and the second is the lattice QCD theory error. We calculate the ratio $f^{D \rightarrow K}_+(0)/f_{D_s}$ and find $2.986 \pm 0.087$ GeV$^{-1}$ and show that this agrees with experiment.Comment: 23 pages, 31 figures, 11 tables. Added a paragraph in sction VII, and updated with PDG 2010 instead of PDG 200

Functional Enhancement of Electrofusion-derived BRIN-BD11 Insulin-secreting Cells After Implantation into Diabetic Mice

Electrofusion-derived BRIN-BD11 cells are glucosesensitive insulin-secreting cells which provide an archetypal bioengineered surrogate β-cell for insulin replacement therapy in diabetes mellitus, 5x106 BRIN-BD11 cells were implanted intraperitoneally into severely hyperglycaemic (>24mmol/l) streptozotocin-induced insulin-treated diabetic athymic nude (nu/nu) mice. The implants reduced hyperglycaemia such that insulin injections were discontinued by 5–16 days (<17mmol/l) and normoglycaemia (<9mmol/l) was achieved by 7–20 days. Implanted cells were removed after 28 days and re-established in culture. After re-culture for 20 days, glucose-stimulated (16.7mmol/l) insulin release was enhanced by 121% (p<0.001) compared to non-implanted cells. Insulin responses to glucagon-like peptide-1 (10−9mol/l), cholecystokinin-8 (10−8 mol/l) and L-alanine (10 mmol/l) were increased by 32%, 31% and 68% respectively (p<0.05–0.01). Insulin content of the cells was 148% greater at 20 days after re-culture than before implantation (p<0.001), but basal insulin release (at 5.6 mmol/l glucose) was not changed. After re-culture for 40 days, insulin content declined to 68% of the content before implantation (p<0.01), although basal insulin release was unchanged. However, the insulin secretory responses to glucose, glucagonlike peptide-1, cholecystokinin-8 and L-alanine were decreased after 40 days of re-culture to 65%, 72%, 73% and 42% respectively of the values before implantation (p<0.05–0.01). The functional enhancement of electrofusion-derived surrogate β-cells that were re-cultured for 20 days after implantation and restoration of normoglycaemia indicates that the in vivo environment could greatly assist β-cell engineering approaches to therapy for diabetes

Regulation of development by Rx genes

The paired-like homeobox-containing gene Rx has a critical role in the eye development of several vertebrate species including Xenopus, mouse, chicken, medaka, zebrafish and human. Rx is initially expressed in the anterior neural region of developing embryos, and later in the retina and ventral hypothalamus. Abnormal regulation or function of Rx results in severe abnormalities of eye formation. Overexpression of Rx in Xenopus and zebrafish embryos leads to overproliteration of retinal cells. A targeted elimination of Rx in mice results in a lack of eye formation. Mutations in Rx genes are the cause of the mouse mutation eyeless (ey1), the medaka temperature sensitive mutation eyeless (el) and the zebrafish mutation chokh. In humans, mutations in Rx lead to anophthalmia. All of these studies indicate that Rx genes are key factors in vertebrate eye formation. Because these results cannot be easily reconciled with the most popular dogmas of the field, we offer our interpretation of eye development and evolution

Scenario planning for the Edinburgh city region

This paper examines the application of scenario planning techniques to the detailed and daunting challenge of city re-positioning when policy makers are faced with a heavy history and a complex future context. It reviews a process of scenario planning undertaken in the Edinburgh city region, exploring the scenario process and its contribution to strategies and policies for city repositioning. Strongly rooted in the recent literature on urban and regional economic development, the text outlines how key individuals and organisations involved in the process participated in far-reaching analyses of the possible future worlds in which the Edinburgh city region might find itself

Bifurcation and fine structure phenomena in critical collapse of a self-gravitating σ\sigma-field

Building on previous work on the critical behavior in gravitational collapse of the self-gravitating SU(2) $\sigma$-field and using high precision numerical methods we uncover a fine structure hidden in a narrow window of parameter space. We argue that this numerical finding has a natural explanation within a dynamical system framework of critical collapse

Evidence for independent Hox gene duplications in the hagfish lineage: a PCR-based gene inventory of Eptatretus stoutii

Hox genes code for transcription factors that play a major role in the development of all animal phyla. In invertebrates these genes usually occur as tightly linked cluster, with a few exceptions where the clusters have been dissolved. Only in vertebrates multiple clusters have been demonstrated which arose by duplication from a single ancestral cluster. This history of Hox cluster duplications, in particular during the early elaboration of the vertebrate body plan, is still poorly understood. In this paper we report the results of a PCR survey on genomic DNA of the pacific hagfish Eptatretus stoutii. Hagfishes are one of two clades of recent jawless fishes that are an offshoot of the early radiation of jawless vertebrates. Our data provide evidence for at least 33 distinct Hox genes in the hagfish genome, which is most compatible with the hypothesis of multiple Hox clusters. The largest number, seven, of distinct homeobox fragments could be assigned to paralog group 9, which could imply that the hagfish has more than four clusters. Quartet mapping reveals that within each paralog group the hagfish sequences are statistically more closely related to gnathostome Hox genes than with either amphioxus or lamprey genes. These results support two assumptions about the history of Hox genes: (1) The association of hagfish homeobox sequences with gnathostome sequences suggests that at least one Hox cluster duplication event happened in the stem of vertebrates, i.e., prior to the most recent common ancestor of jawed and jawless vertebrates. (2) The high number of paralog group 9 sequences in hagfish and the phylogenetic position of hagfish suggests that the hagfish lineage underwent additional independent Hox cluster/-gene duplication events