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Abstract
Stage 55, T3 exposure for 12 hours.
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Abstract
stage 55 control samples, No T3 Exposure.
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Abstract
Stage 55, T3 exposure for 12 hours.
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Abstract
adult frog no T3 treatment.
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Abstract
adult frog no T3 treatment.
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Abstract
Stage 55, T3 exposure for 48 hours.
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Abstract
MgSiO3 akimotoite is stable relative to majorite-garnet under low-temperature geotherms within steeply or rapidly subducting slabs. Two compositions of Mg-akimotoite were synthesized under similar conditions: Z674 (containing about 550 ppm wt H2O) was synthesized at 22 GPa and 1,500 A degrees C and SH1101 (nominally anhydrous) was synthesized at 22 GPa and 1,250 A degrees C. Crystal structures of both samples differ significantly from previous studies to give slightly smaller Si sites and larger Mg sites. The bulk thermal expansion coefficients of Z674 are (153-839 K) of a (1) = 20(3) x 10(-9) K-2 and a (0) = 17(2) x 10(-6) K-1, with an average of alpha (0) = 27.1(6) x 10(-6) K-1. Compressibility at ambient temperature of Z674 was measured up to 34.6 GPa at Sector 13 (GSECARS) at Advanced Photon Source Argonne National Laboratory. The second-order Birch-Murnaghan equation of state (BM2 EoS) fitting yields: V (0) = 263.7(2) (3), K (T0) = 217(3) GPa (K' fixed at 4). The anisotropies of axial thermal expansivities and compressibilities are similar: alpha (a) = 8.2(3) and alpha (c) = 10.68(9) (10(-6) K-1); beta (a) = 11.4(3) and beta (c) = 15.9(3) (10(-4) GPa). Hydration increases both the bulk thermal expansivity and compressibility, but decreases the anisotropy of structural expansion and compression. Complementary Raman and Fourier transform infrared (FTIR) spectroscopy shows multiple structural hydration sites. Low-temperature and high-pressure FTIR spectroscopy (15-300 K and 0-28 GPa) confirms that the multiple sites are structurally unique, with zero-pressure intrinsic anharmonic mode parameters between -1.02 x 10(-5) and +1.7 x 10(-5) K-1, indicating both weak hydrogen bonds (O-H center dot center dot center dot O) and strong OH bonding due to long O center dot center dot center dot O distances.
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Abstract
During the climax of amphibian metamorphosis many tadpole organs remodel. The different remodeling strategies are controlled by thyroid hormone (TH). The liver, skin, and tail fibroblasts shut off tadpole genes and activate frog genes in the same cell without DNA replication. We refer to this as "gene switching". In contrast, the exocrine pancreas and the intestinal epithelium dedifferentiate to a progenitor state and then redifferentiate to the adult cell type. Tadpole and adult globin are not present in the same cell. Switching from red cells containing tadpole-specific globin to those with frog glob it in the liver occurs at a progenitor cell stage of development and is preceded by DNA replication. Red cel switching is the only one of these remodeling strategies that resembles a stem cell mechanism. (C) 2009 Elsevier Inc. All rights reserved.
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Abstract
Thyroid hormone (TH) controlled gene expression profile shave been studied in the tail, hind limb and brain tissues during TH-induced and spontaneous Xenopus laevis metamorphosis. Amplified cRNA probes mixed with a universal standard were hybridized to a set of 21,807 strand 60-mer oligonucleotides on each slide representing the entries in X laevis UniGene Build 48. Most of the up-regulated genes in hind limb and brain are the same. This reflects in part the fact that the initial response to TH induction in both tissues is cell proliferation. A large number of up-regulated genes in the limb and brain programs encode common components of the cell cycle, DNA and RNA metabolism, transcription and translation. Notch is one of the few genes that is differentially expressed exclusively in the brain in the first 48 h of TH induction studied in these experiments. The TH-induced gene expression changes in the tail are different from the limb and brain programs. Distinct muscle and fibroblast programs were identified in the tail. Dying muscle fibers in tail (marked by active caspase-3) up-regulate a group of genes that include proteolytic enzymes. At the climax of metamorphosis, tail muscle down-regulates more than half of the genes that encode the glycolytic enzymes in the cytoplasm and the tricarboxylic acid pathway and all five complexes of the electron transport system in mitochondria. These changes in gene expression precede the activation of caspase-3. Some of these same energy metabolism-retated genes are up-regulated in the limb and brain programs by TH. A prominent feature of the tail fibroblasts is the down-regulation of several collagen and other extra cellular matrix genes and the up-regulation of hydrolytic enzymes that are responsible for dissolving the notochord and resorbing the tail. (C) 2005 Elsevier Inc. All rights reserved.
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Abstract
Transgenic Xenopus laevis tadpoles that express a dominant negative form of the thyroid hormone receptor (TRDN) controlled by the cardiac actin muscle promoter (pCar) develop with very little limb muscle. Under the control of the tetracycline system the transgene can be induced at will by adding doxycycline to the rearing water. Pre-existing limb muscle fibers begins to disintegrate within 2 days after up-regulation of the TRDN transgene. The muscle cells do not die even after weeks of transgene exposure when the myofibrils have degenerated completely and the tadpole is nearing death. A microarray analysis after 2 weeks of exposure to the transgene identified 24 muscle genes whose expression was altered in such a way that they might cause the muscle phenotype. These candidate genes are normally activated in growing limb muscle but they are repressed by the TRDN transgene. Several of these genes have been implicated in mammalian myopathies. However, the expression of only one of these genes, calsequestrin, is down-regulated in I day and therefore might initiate the degeneration. Calsequestrin is one of several affected genes that encode proteins involved in calcium sequestration, transport and utilization in muscle suggesting that uncontrolled calcium influx into the growing limb muscle fibers causes rhabdomyolysis. Many of the same genes that are down-regulated in the tail at the peak of metamorphic climax just before it is resorbed are suppressed in the transgenic limb muscle in effect turning the limb growth program into a tail resorption program. (c) 2006 Elsevier Inc. All rights reserved.
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