2,898 research outputs found
Classical Conformal Blocks and Accessory Parameters from Isomonodromic Deformations
Classical conformal blocks naturally appear in the large central charge limit
of 2D Virasoro conformal blocks. In the correspondence, they
are related to classical bulk actions and are used to calculate entanglement
entropy and geodesic lengths. In this work, we discuss the identification of
classical conformal blocks and the Painlev\'e VI action showing how
isomonodromic deformations naturally appear in this context. We recover the
accessory parameter expansion of Heun's equation from the isomonodromic
-function. We also discuss how the expansion of the
-function leads to a novel approach to calculate the 4-point classical
conformal block.Comment: 32+10 pages, 2 figures; v3: upgraded notation, discussion on moduli
space and monodromies, numerical and analytic checks; v2: added refs, fixed
emai
MYC-type transcription factors, MYC67 and MYC70, interact with ICE1 and negatively regulate cold tolerance in Arabidopsis
The expression of hundreds of genes is induced by low temperatures via a cold signaling pathway. ICE1, a MYC-type transcription factor, plays an important role in the induction of CBF3/DREB1A to control cold-responsive genes and cold tolerance. To elucidate other molecular factors, a yeast 2-hybrid screening was performed. Two MYC-type transcription factors, MYC67 and MYC70, were identified as ICE1-interacting proteins. The myc mutants were more tolerant to freezing temperatures than wild type. CBF3/DREB1A and other cold-responsive genes were up-regulated in the myc mutants. Overexpression of the MYC genes increased the cold sensitivity and down-regulated the expression of cold-responsive genes. The MYC proteins interacted with the cis-elements in the CBF3/DREB1A promoter, probably to interfere interaction between ICE1 and the cis-elements. Taken together, these results demonstrate that MYC67 and MYC70, ICE1 interactors, negatively regulate cold-responsive genes and cold tolerance
Suture Materials, 1980s: Properties, Uses, and Abuses
Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/66057/1/j.1365-4362.1982.tb03154.x.pd
Dynamic Analysis of Vascular Morphogenesis Using Transgenic Quail Embryos
Background: One of the least understood and most central questions confronting biologists is how initially simple clusters or sheet-like cell collectives can assemble into highly complex three-dimensional functional tissues and organs. Due to the limits of oxygen diffusion, blood vessels are an essential and ubiquitous presence in all amniote tissues and organs. Vasculogenesis, the de novo self-assembly of endothelial cell (EC) precursors into endothelial tubes, is the first step in blood vessel formation [1]. Static imaging and in vitro models are wholly inadequate to capture many aspects of vascular pattern formation in vivo, because vasculogenesis involves dynamic changes of the endothelial cells and of the forming blood vessels, in an embryo that is changing size and shape.
Methodology/Principal Findings: We have generated Tie1 transgenic quail lines Tg(tie1:H2B-eYFP) that express H2B-eYFP in all of their endothelial cells which permit investigations into early embryonic vascular morphogenesis with unprecedented clarity and insight. By combining the power of molecular genetics with the elegance of dynamic imaging, we follow the precise patterning of endothelial cells in space and time. We show that during vasculogenesis within the vascular plexus, ECs move independently to form the rudiments of blood vessels, all while collectively moving with gastrulating tissues that flow toward the embryo midline. The aortae are a composite of somatic derived ECs forming its dorsal regions and the splanchnic derived ECs forming its ventral region. The ECs in the dorsal regions of the forming aortae exhibit variable mediolateral motions as they move rostrally; those in more ventral regions show significant lateral-to-medial movement as they course rostrally.
Conclusions/Significance: The present results offer a powerful approach to the major challenge of studying the relative role(s) of the mechanical, molecular, and cellular mechanisms of vascular development. In past studies, the advantages of the molecular genetic tools available in mouse were counterbalanced by the limited experimental accessibility needed for imaging and perturbation studies. Avian embryos provide the needed accessibility, but few genetic resources. The creation of transgenic quail with labeled endothelia builds upon the important roles that avian embryos have played in previous studies of vascular development
Effects of the Molecular Weight and the Degree of Deacetylation of Chitosan Oligosaccharides on Antitumor Activity
Effects of the degree of deacetylation (DDA) and the molecular mass of chitosan oligosaccharides (CTS-OS), obtained from the enzymatic hydrolysis of high molecular weight chitosan (HMWC), on antitumor activity was explored. The DDA and molecular weights of CTS-OS were determined by matrix-assisted laser desorption/ionization-mass spectrometry (MALDI-TOF MS) analysis. The CTS-OS were found to be a mixture of mainly dimers (18.8%), trimers (24.8%), tetramers (24.9%), pentamers (17.7%), hexamers (7.1%), heptamers (3.3%), and octamers (3.4%). The CTS-OS were further fractionated by gel-filtration chromatography into two major fractions: (1) COS, consisting of glucosamine (GlcN)n, n = 3–5 with DDA 100%; and (2) HOS, consisting of (GlcN)5 as the minimum residues and varying number of N-acetylglucosamine (GlcNAc)n, n = 1–2 with DDA about 87.5% in random order. The cytotoxicities, expressed as the concentration needed for 50% cell death (CC50), of CTS-OS, COS, and HOS against PC3 (prostate cancer cell), A549 (lung cancer cell), and HepG2 (hepatoma cell), were determined to be 25 μg·mL−1, 25 μg·mL−1, and 50 μg·mL−1, respectively. The HMWC was approximately 50% less effective than both CTS-OS and COS. These results demonstrate that the molecular weight and DDA of chitosan oligosaccharides are important factors for suppressing cancer cell growth
The Effect of p38 Mitogen-Activated Protein Kinase Activation on Inflammatory Liver Damage following Hemorrhagic Shock in Rats
Hemorrhagic shock is a frequent cause of liver failure and often leads to a fatal outcome. Several studies have revealed that p38 MAPK is a key mediator in hemorrhagic damage of the primary organs through the activation of proinflammatory cytokines such as tumor necrosis factor (TNF)-α and interleukin (IL)-1β. However, the precise role of these factors in liver damage following hemorrhagic shock is unclear. In this study, we used FR167653, a specific inhibitor of p38 MAPK phosphorylation, to examine the role of p38 MAPK in liver damage occurring up to 5 hours after a hemorrhagic episode in a rat model. Activation of p38 MAPK in the liver as well as an increase in hepatic mRNA expression and serum concentrations of TNF-α and IL-1β occurred during the early phase after hemorrhage. Increased serum levels of hepatic enzymes, as well as histological damage and activated neutrophil accumulation in the liver, were observed in the late phase following hemorrhagic shock. FR167653 inhibited the inflammation-related hepatic injury following hemorrhagic shock. Bacterial lipopolysaccharide (LPS) derived from the gut appeared to have little effects on the hepatic damage. These results demonstrate that p38 MAPK activation is induced by hepatic ischemia during hemorrhagic shock and plays an important role both in the hepatic expression of proinflammatory cytokines and in the development of inflammation-related liver damage
Determination of nonthermal bonding origin of a novel photoexcited lattice instability in SnSe
Interatomic forces that bind materials are largely determined by an often
complex interplay between the electronic band-structure and the atomic
arrangements to form its equilibrium structure and dynamics. As these forces
also determine the phonon dispersion, lattice dynamics measurements are often
crucial tools for understanding how materials transform between different
structures. This is the case for the mono-chalcogenides which feature a number
of lattice instabilities associated with their network of resonant bonds and a
large tunability in their functional properties. SnSe hosts a novel lattice
instability upon above-bandgap photoexcitation that is distinct from the
distortions associated with its high temperature phase transition,
demonstrating that photoexcitation can alter the interatomic forces
significantly different than thermal excitation. Here we report decisive
time-resolved X-ray scattering-based measurements of the nonequlibrium lattice
dynamics in SnSe. By fitting interatomic force models to the excited-state
dispersion, we determine this instability as being primarily due to changes in
the fourth-nearest neighbor bonds that connect bilayers, with relatively little
change to the intralayer resonant bonds. In addition to providing critical
insight into the nonthermal bonding origin of the instability in SnSe, such
measurements will be crucial for understanding and controlling materials
properties under non-equilibrium conditions
Momentum and Coordinate Space Three-nucleon Potentials
In this paper we give explicit formulae in momentum and coordinate space for
the three-nucleon potentials due to and meson exchange, derived
from off-mass-shell meson-nucleon scattering amplitudes which are constrained
by the symmetries of QCD and by the experimental data. Those potentials have
already been applied to nuclear matter calculations. Here we display additional
terms which appear to be the most important for nuclear structure. The
potentials are decomposed in a way that separates the contributions of
different physical mechanisms involved in the meson-nucleon amplitudes. The
same type of decomposition is presented for the TM force: the
, the chiral symmetry breaking and the nucleon pair terms are isolated.Comment: LATEX, 33 pages, 3 figures (available as postscript files upon
request
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