Sloshing in High Speed Galaxy Interactions

Observations of lopsided spiral galaxies motivated us to explore whether the rapid passage of a companion galaxy could cause them. We examine whether the center of mass of the visible matter becomes displaced from the center of mass of the dark halo during the intruder's passage, thereby causing an asymmetric response and asymmetric structure. Two dimensional $N$-body simulations indicate that this can happen. We also explore some consequences of this offset. These include the center of mass of the visible disk following a decaying orbit around the halo center of mass and the development of transient one-armed spirals that persist for up to six rotation periods. We then study the results of a variety of initial conditions based on such offsets. We report on the results of several runs in which we initially offset a disk from its halo's center of mass by an amount typical of the above interaction. In some runs the halo is free to move, while in others it is held fixed. We used three different mass distributions for the halo in these runs. We find that the disk's center of mass spiraled inward creating a variety of observed or observable phenomena including one-armed spirals, massive clumps of particles, and counter-rotating waves. The systems settle into relatively axisymmetric configurations. Whether or not the end states included a bar depended on a variety of initial conditions.Comment: 20 text pages, 3 tables, 24 figures. A gzipped postscripped version with higher resolution figures can be downloaded from http://butch.umephy.maine.edu/kickers/Research/Sloshing/ . Accepted for publication in The Astrophysical Journa

Negative Energy and Angular Momentum Modes of Thin Accretion Disks

This work derives the linearized equations of motion, the Lagrangian density, the Hamiltonian density, and the canonical angular momentum density for general perturbations [$\propto \exp(im\phi)$ with $m=0,\pm 1,..$] of a geometrically thin self-gravitating, homentropic fluid disk including the pressure. The theory is applied to ``eccentric,'' $m=\pm 1$ perturbations of a geometrically thin Keplerian disk. We find $m=1$ modes at low frequencies relative to the Keplerian frequency. Further, it shown that these modes can have negative energy and negative angular momentum. The radial propagation of these low frequency $m=1$ modes can transport angular momentum away from the inner region of a disk and thus increase the rate of mass accretion. Depending on the radial boundary conditions there can be discrete low-frequency, negative-energy, $m=1$ modes.Comment: 24 pages, 8 figure

NM23 proteins: innocent bystanders or local energy boosters for CFTR?

NM23 proteins NDPK-A and -B bind to the cystic fibrosis (CF) protein CFTR in different ways from kinases such as PKA, CK2 and AMPK or linkers to cell calcium such as calmodulin and annexins. NDPK-A (not -B) interacts with CFTR through reciprocal AMPK binding/control, whereas NDPK-B (not -A) binds directly to CFTR. NDPK-B can activate G proteins without ligand-receptor coupling, so perhaps NDPK-B's binding influences energy supply local to a nucleotide-binding site (NBD1) needed for CFTR to function. Curiously, CFTR (ABC-C7) is a member of the ATP-binding cassette (ABC) protein family that does not obey 'clan rules'; CFTR channels anions and is not a pump, regulates disparate processes, is itself regulated by multiple means and is so pleiotropic that it acts as a hub that orchestrates calcium signaling through its consorts such as calmodulin/annexins. Furthermore, its multiple partners make CFTR dance to different tunes in different cellular and subcellular locations as it recycles from the plasma membrane to endosomes. CFTR function in airway apical membranes is inhibited by smoking which has been dubbed 'acquired CF'. CFTR alone among family members possesses a trap for other proteins that it unfurls as a 'fish-net' and which bears consensus phosphorylation sites for many protein kinases, with PKA being the most canonical. Recently, the site of CFTR's commonest mutation has been proposed as a knock-in mutant that alters allosteric control of kinase CK2 by log orders of activity towards calmodulin and other substrates after CFTR fragmentation. This link from CK2 to calmodulin that binds the R region invokes molecular paths that control lumen formation, which is incomplete in the tracheas of some CF-affected babies. Thus, we are poised to understand the many roles of NDPK-A and -B in CFTR function and, especially lumen formation, which is defective in the gut and lungs of many CF babies

Porady i ostrzeżenia dla projektanta systemu CANopen

Although the CANopen application layer is well specified, the system designer could make failures or misuse the services and protocols. This is not only possible for the application layer, but also for the data link and the physical layer. This paper provides some hints and kinks designing CANopen network system.Chociaż magistrala CANopen jest dobrze wyspecyfikowana, to jednak projektant systemu może popełnić pomyłki lub błędnie zastosować usługi i protokoły. Może się to zdarzyć nie tylko w warstwie aplikacji, ale także w łączu danych i w warstwie fizycznej. W artykule przedstawiono niektóre porady i ostrzeżenia przydatne w projektowaniu systemu sieciowego CANopen

Revertant mutants modify, but do not rescue, the gating defect of the cystic fibrosis mutant G551D-CFTR

Cystic fibrosis (CF) is caused by dysfunction of the epithelial anion channel cystic fibrosis transmembrane conductance regulator (CFTR). One strategy to restore function to CF mutants is to suppress defects in CFTR processing and function using revertant mutations. Here, we investigate the effects of the revertant mutations G550E and 4RK (the simultaneous disruption of four arginine-framed tripeptides (AFTs): R29K, R516K, R555K and R766K) on the CF mutant G551D, which impairs severely channel gating without altering protein processing and which affects a residue in the same α-helix as G550 and R555. Both G550E and 4RK augmented strongly CFTR-mediated iodide efflux from BHK cells expressing G551D-CFTR. To learn how revertant mutations influence G551D-CFTR function, we studied protein processing and single-channel behaviour. Neither G550E nor 4RK altered the expression and maturation of G551D-CFTR protein. By contrast, both revertants had marked effects on G551D-CFTR channel gating, increasing strongly opening frequency, while 4RK also diminished noticeably the duration of channel openings. Because G551D-CFTR channel gating is ATP independent, we investigated whether revertant mutations restore ATP dependence to G551D-CFTR. Like wild-type CFTR, the activity of 4RK-G551D-CFTR varied with ATP concentration, suggesting that 4RK confers some ATP dependence on the G551D-CFTR channel. Thus, the revertant mutations G550E and 4RK alter the gating pattern and ATP dependence of G551D-CFTR without restoring single-channel activity to wild-type levels. Based on their impact on the CF mutants F508del and G551D, we conclude that G550E and 4RK have direct effects on CFTR structure, but that their action on CFTR processing and channel function is CF mutation specific

Application of high-resolution single-channel recording to functional studies of cystic fibrosis mutants

The patch-clamp technique is a powerful and versatile method to investigate the cystic fibrosis transmem-brane conductance regulator (CFTR) Cl(−) channel, its malfunction in disease and modulation by small molecules. Here, we discuss how the molecular behaviour of CFTR is investigated using high-resolution single-channel recording and kinetic analyses of channel gating. We review methods used to quantify how cystic fibrosis (CF) mutants perturb the biophysical properties and regulation of CFTR. By explaining the relationship between macroscopic and single-channel currents, we demonstrate how single-channel data provide molecular explanations for changes in CFTR-mediated transepithelial ion transport elicited by CF mutants