Non-universal Efimov Atom-Dimer Resonances in a Three-Component Mixture of 6Li

We observed an enhanced atom-dimer relaxation due to the existence of Efimov states in a three-component mixture of 6Li atoms. We measured the magnetic-field dependence of the atom-dimer loss coefficient in the mixture of atoms in state |1> and dimers formed in states |2> and |3>, and found two peaks corresponding to the degeneracy points of the |23> dimer energy level and energy levels of Efimov trimers. We found that the locations of these peaks disagree with universal theory predictions, in a way that cannot be explained by non-universal two-body properties. We constructed theoretical models that characterize the non-universal three-body physics of three-component 6Li atoms in the low energy domain.Comment: 5 pages, 3 figure

Flow Equation for Supersymmetric Quantum Mechanics

We study supersymmetric quantum mechanics with the functional RG formulated in terms of an exact and manifestly off-shell supersymmetric flow equation for the effective action. We solve the flow equation nonperturbatively in a systematic super-covariant derivative expansion and concentrate on systems with unbroken supersymmetry. Already at next-to-leading order, the energy of the first excited state for convex potentials is accurately determined within a 1% error for a wide range of couplings including deeply nonperturbative regimes.Comment: 24 pages, 8 figures, references added, typos correcte

Small‐Molecule Activators of Glucose‐6‐phosephate Dehydrogenase (G6PD) Bridging the Dimer Interface

We have recently identified AG1, a small-molecule activator that functions by promoting oligomerization of glucose-6- phosphate dehydrogenase (G6PD) to the catalytically competent forms. Biochemical experiments indicate activation of G6PD by the original hit molecule (AG1) is noncovalent and that one C2-symmetric region of the G6PD homodimer is important for ligand function. Consequently, the disulfide in AG1 is not required for activation of G6PD and a number of analogs were prepared without this reactive moiety. Our Study supports a mechanism of action whereby AG1 bridges the dimer interface at the structural nicotinamide adenine dinucleotide phosphate (NADP+)-binding sites of two interacting G6PD monomers. Small molecules that promote G6PD oligomerization have the potential to provide a first-in-class treatment for G6PD deficiency. This general strategy could be applied to other enzyme deficiencies where control of oligomerization can enhance enzymatic activity and/or stability

Heat-induced SIRT1-mediated H4K16ac deacetylation impairs resection and SMARCAD1 recruitment to double strand breaks

Hyperthermia inhibits DNA double-strand break (DSB) repair that utilizes homologous recombination (HR) pathway by a poorly defined mechanism(s); however, the mechanisms for this inhibition remain unclear. Here we report that hyperthermia decreases H4K16 acetylation (H4K16ac), an epigenetic modification essential for genome stability and transcription. Heat-induced reduction in H4K16ac was detected in humans

Genome-wide distribution of histone H4 Lysine 16 acetylation sites and their relationship to gene expression

BACKGROUND: Histone post-translational modifications are critical determinants of chromatin structure and function, impacting multiple biological processes including DNA transcription, replication, and repair. The post-translational acetylation of histone H4 at lysine 16 (H4K16ac) was initially identified in association with dosage compensation of the Drosophila male X chromosome. However, in mammalian cells, H4K16ac is not associated with dosage compensation and the genomic distribution of H4K16ac is not precisely known. Therefore, we have mapped the genome-wide H4K16ac distribution in human cells. RESULTS: We performed H4K16ac chromatin immunoprecipitation from human embryonic kidney 293 (HEK293) cells followed by hybridization to whole-genome tiling arrays and identified 25,893 DNA regions (false discovery rate <0.005) with average length of 692 nucleotides. Interestingly, although a majority of H4K16ac sites localized within genes, only a relatively small fraction (~10%) was found near promoters, in contrast to the distribution of the acetyltransferase, MOF, responsible for acetylation at K16 of H4. Using differential gene expression profiling data, 73 genes (> ±1.5-fold) were identified as potential H4K16ac-regulated genes. Seventeen transcription factor-binding sites were significantly associated with H4K16ac occupancy (p < 0.0005). In addition, a consensus 12-nucleotide guanine-rich sequence motif was identified in more than 55% of the H4K16ac peaks. CONCLUSIONS: The results suggest that H4K16 acetylation has a limited effect on transcription regulation in HEK293 cells, whereas H4K16ac has been demonstrated to have critical roles in regulating transcription in mouse embryonic stem cells. Thus, H4K16ac-dependent transcription regulation is likely a cell type specific process

Novel diffusion mechanism on the GaAs(001) surface: the role of adatom-dimer interaction

Employing first principles total energy calculations we have studied the behavior of Ga and Al adatoms on the GaAs(001)-beta2 surface. The adsorption site and two relevant diffusion channels are identified. The channels are characterized by different adatom-surface dimer interaction. Both affect in a novel way the adatom migration: in one channel the diffusing adatom jumps across the surface dimers and leaves the dimer bonds intact, in the other one the surface dimer bonds are broken. The two channels are taken into account to derive effective adatom diffusion barriers. From the diffusion barriers we conclude a strong diffusion anisotropy for both Al and Ga adatoms with the direction of fastest diffusion parallel to the surface dimers. In agreement with experimental observations we find higher diffusion barriers for Al than for Ga.Comment: 4 pages, 2 figures, Phys. Rev. Lett. 79 (1997). Other related publications can be found at http://www.rz-berlin.mpg.de/th/paper.htm

Correcting Glucose-6-Phosphate Dehydrogenase Deficiency with a Small-Molecule Activator

Glucose-6-phosphate dehydrogenase (G6PD) deficiency, one of the most common human genetic enzymopathies, is caused by over 160 different point mutations and contributes to the severity of many acute and chronic diseases associated with oxidative stress, including hemolytic anemia and bilirubin-induced neurological damage particularly in newborns. As no medications are available to treat G6PD deficiency, here we seek to identify a small molecule that corrects it. Crystallographic study and mutagenesis analysis identify the structural and functional defect of one common mutant (Canton, R459L). Using high-throughput screening, we subsequently identify AG1, a small molecule that increases the activity of the wild-type, the Canton mutant and several other common G6PD mutants. AG1 reduces oxidative stress in cells and zebrafish. Furthermore, AG1 decreases chloroquine- or diamide-induced oxidative stress in human erythrocytes. Our study suggests that a pharmacological agent, of which AG1 may be a lead, will likely alleviate the challenges associated with G6PD deficiency

Phase Transition in \nu=2 Bilayer Quantum Hall State

The Hall-plateau width and the activation energy were measured in the bilayer quantum Hall state at filling factor \nu=2, 1 and 2/3, by changing the total electron density and the density ratio in the two quantum wells. Their behavior are remarkably different from one to another. The \nu=1 state is found stable over all measured range of the density difference, while the \nu=2/3$ state is stable only around the balanced point. The \nu=2 state, on the other hand, shows a phase transition between these two types of the states as the electron density is changed.Comment: 5 pages including figures, RevTe

Exploring the Thermodynamics of a Universal Fermi Gas

From sand piles to electrons in metals, one of the greatest challenges in modern physics is to understand the behavior of an ensemble of strongly interacting particles. A class of quantum many-body systems such as neutron matter and cold Fermi gases share the same universal thermodynamic properties when interactions reach the maximum effective value allowed by quantum mechanics, the so-called unitary limit [1,2]. It is then possible to simulate some astrophysical phenomena inside the highly controlled environment of an atomic physics laboratory. Previous work on the thermodynamics of a two-component Fermi gas led to thermodynamic quantities averaged over the trap [3-5], making it difficult to compare with many-body theories developed for uniform gases. Here we develop a general method that provides for the first time the equation of state of a uniform gas, as well as a detailed comparison with existing theories [6,14]. The precision of our equation of state leads to new physical insights on the unitary gas. For the unpolarized gas, we prove that the low-temperature thermodynamics of the strongly interacting normal phase is well described by Fermi liquid theory and we localize the superfluid transition. For a spin-polarized system, our equation of state at zero temperature has a 2% accuracy and it extends the work of [15] on the phase diagram to a new regime of precision. We show in particular that, despite strong correlations, the normal phase behaves as a mixture of two ideal gases: a Fermi gas of bare majority atoms and a non-interacting gas of dressed quasi-particles, the fermionic polarons [10,16-18].Comment: 8 pages, 5 figure