Rotation-induced 3D vorticity in 4He superfluid films adsorbed on a porous glass

Detailed study of torsional oscillator experiments under steady rotation up to 6.28 rad/sec is reported for a 4He superfluid monolayer film formed in 1 micrometer-pore diameter porous glass. We found a new dissipation peak with the height being in proportion to the rotation speed, which is located to the lower temperature than the vortex pair unbinding peak observed in the static state. We propose that 3D coreless vortices ("pore vortices") appear under rotation to explain this new peak. That is, the new peak originates from dissipation close to the pore vortex lines, where large superfluid velocity shifts the vortex pair unbinding dissipation to lower temperature. This explanation is confirmed by observation of nonlinear effects at high oscillation amplitudes.Comment: 4pages, 5figure

Onset of Superfluidity in 4He Films Adsorbed on Disordered Substrates

We have studied 4He films adsorbed in two porous glasses, aerogel and Vycor, using high precision torsional oscillator and DC calorimetry techniques. Our investigation focused on the onset of superfluidity at low temperatures as the 4He coverage is increased. Torsional oscillator measurements of the 4He-aerogel system were used to determine the superfluid density of films with transition temperatures as low as 20 mK. Heat capacity measurements of the 4He-Vycor system probed the excitation spectrum of both non-superfluid and superfluid films for temperatures down to 10 mK. Both sets of measurements suggest that the critical coverage for the onset of superfluidity corresponds to a mobility edge in the chemical potential, so that the onset transition is the bosonic analog of a superconductor-insulator transition. The superfluid density measurements, however, are not in agreement with the scaling theory of an onset transition from a gapless, Bose glass phase to a superfluid. The heat capacity measurements show that the non-superfluid phase is better characterized as an insulator with a gap.Comment: 15 pages (RevTex), 21 figures (postscript

Rapid Transcriptional Pulsing Dynamics of High Expressing Retroviral Transgenes in Embryonic Stem Cells

Single cell imaging studies suggest that transcription is not continuous and occurs as discrete pulses of gene activity. To study mechanisms by which retroviral transgenes can transcribe to high levels, we used the MS2 system to visualize transcriptional dynamics of high expressing proviral integration sites in embryonic stem (ES) cells. We established two ES cell lines each bearing a single copy, self-inactivating retroviral vector with a strong ubiquitous human EF1α gene promoter directing expression of mRFP fused to an MS2-stem-loop array. Transfection of MS2-EGFP generated EGFP focal dots bound to the mRFP-MS2 stem loop mRNA. These transcription foci colocalized with the transgene integration site detected by immunoFISH. Live tracking of single cells for 20 minutes detected EGFP focal dots that displayed frequent and rapid fluctuations in transcription over periods as short as 25 seconds. Similarly rapid fluctuations were detected from focal doublet signals that colocalized with replicated proviral integration sites by immunoFISH, consistent with transcriptional pulses from sister chromatids. We concluded that retroviral transgenes experience rapid transcriptional pulses in clonal ES cell lines that exhibit high level expression. These events are directed by a constitutive housekeeping gene promoter and may provide precedence for rapid transcriptional pulsing at endogenous genes in mammalian stem cells

Suppression of Superfluidity of 4^4He in a Nanoporous Glass by Preplating a Kr Layer

Helium in nanoporous media has attracted much interest as a model Bose system with disorder and confinement. Here we have examined how a change in porous structure by preplating a monolayer of krypton affects the superfluid properties of $^4$He adsorbed or confined in a nanoporous Gelsil glass, which has a three-dimensional interconnected network of nanopores of 5.8 nm in diameter. Isotherms of adsorption and desorption of nitrogen show that monolayer preplating of Kr decreases the effective pore diameter to 4.7 nm and broadens the pore size distribution by about eight times from the sharp distribution of the bare Gelsil sample. The superfluid properties were studied by a torsional oscillator for adsorbed film states and pressurized liquid states, both before and after the monolayer Kr preplating. In the film states, both the superfluid transition temperature $T_{\mathrm c}$ and the superfluid density decrease about 10 percent by Kr preplating. The suppression of film superfluidity is attributed to the quantum localization of $^4$He atoms by the randomness in the substrate potential, which is caused by the preplating--induced broadening of the pore size distribution. In the pressurized liquid states, the superfluid density $\rho_{\mathrm s}$ is found to increase by 10 percent by Kr preplating, whereas $T_{\mathrm c}$ is decreased by 2 percent at all pressures. The unexpected enhancement of $\rho_{\mathrm s}$ might indicate the existence of an unknown disorder effect for confined $^4$He.Comment: 27 pages, 8 figures, submitted to J. Phys. Soc. Jp

The Translation Initiation Factor 3f (eIF3f) Exhibits a Deubiquitinase Activity Regulating Notch Activation

The translation initiation factor complex eIF3f has an intrinsic deubiquitinase activity and regulates the Notch signaling pathway

Chronic intermittent hypoxia induces local inflammation of the rat carotid body via functional upregulation of proinflammatory cytokine pathways

Maladaptive changes in the carotid body (CB) induced by chronic intermittent hypoxia (IH) account for the pathogenesis of cardiovascular morbidity in patients with sleep-disordered breathing. We postulated that the proinflammatory cytokines, namely interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α, and cytokine receptors (IL-1r1, gp130 and TNFr1) locally expressed in the rat CB play a pathophysiological role in IH-induced CB inflammation. Results showed increased levels of oxidative stress (serum 8-isoprostane and nitrotyrosine in the CB) in rats with 7-day IH treatment resembling recurrent apneic conditions when compared with the normoxic control. Local inflammation shown by the amount of ED1-containing cells (macrophage infiltration) and the gene transcripts of NADPH oxidase subunits (gp91phox and p22phox) and chemokines (MCP-1, CCR2, MIP-1α, MIP-1β and ICAM-1) in the CB were significantly more in the hypoxic group than in the control. In addition, the cytokines and receptors were expressed in the lobules of chemosensitive glomus cells containing tyrosine hydroxylase and the levels of expressions were significantly increased in the hypoxic group. Exogenous cytokines elevated the intracellular calcium ([Ca2+]i) response to acute hypoxia in the dissociated glomus cells. The effect of cytokines on the [Ca2+]i response was significantly greater in the hypoxic than in the normoxic group. Moreover, daily treatment of IH rats with anti-inflammatory drugs (dexamethasone or ibuprofen) attenuated the levels of oxidative stress, gp91phox expression and macrophage infiltration in the CB. Collectively, these results suggest that the upregulated expression of proinflammatory cytokine pathways could mediate the local inflammation and functional alteration of the CB under chronic IH conditions

Notch and Presenilin Regulate Cellular Expansion and Cytokine Secretion but Cannot Instruct Th1/Th2 Fate Acquisition

Recent reports suggested that Delta1, 4 and Jagged1, 2 possessed the ability to instruct CD4+ T cell into selection of Th1 or Th2 fates, respectively, although the underlying mechanism endowing the cleaved Notch receptor with memory of ligand involved in its activation remains elusive. To examine this, we prepared artificial antigen-presenting cells expressing either DLL1 or Jag1. Although both ligands were efficient in inducing Notch2 cleavage and activation in CD4+ T or reporter cells, the presence of Lunatic Fringe in CD4+ T cells inhibited Jag1 activation of Notch1 receptor. Neither ligand could induce Th1 or Th2 fate choice independently of cytokines or redirect cytokine-driven Th1 or Th2 development. Instead, we find that Notch ligands only augment cytokine production during T cell differentiation in the presence of polarizing IL-12 and IL-4. Moreover, the differentiation choices of naïve CD4+ T cells lacking γ-secretase, RBP-J, or both in response to polarizing cytokines revealed that neither presenilin proteins nor RBP-J were required for cytokine-induced Th1/Th2 fate selection. However, presenilins facilitate cellular proliferation and cytokine secretion in an RBP-J (and thus, Notch) independent manner. The controversies surrounding the role of Notch and presenilins in Th1/Th2 polarization may reflect their role as genetic modifiers of T-helper cells differentiation

Notch and Presenilin Regulate Cellular Expansion and Cytokine Secretion but Cannot Instruct Th1/Th2 Fate Acquisition

Recent reports suggested that Delta1, 4 and Jagged1, 2 possessed the ability to instruct CD4+ T cell into selection of Th1 or Th2 fates, respectively, although the underlying mechanism endowing the cleaved Notch receptor with memory of ligand involved in its activation remains elusive. To examine this, we prepared artificial antigen-presenting cells expressing either DLL1 or Jag1. Although both ligands were efficient in inducing Notch2 cleavage and activation in CD4+ T or reporter cells, the presence of Lunatic Fringe in CD4+ T cells inhibited Jag1 activation of Notch1 receptor. Neither ligand could induce Th1 or Th2 fate choice independently of cytokines or redirect cytokine-driven Th1 or Th2 development. Instead, we find that Notch ligands only augment cytokine production during T cell differentiation in the presence of polarizing IL-12 and IL-4. Moreover, the differentiation choices of naïve CD4+ T cells lacking γ-secretase, RBP-J, or both in response to polarizing cytokines revealed that neither presenilin proteins nor RBP-J were required for cytokine-induced Th1/Th2 fate selection. However, presenilins facilitate cellular proliferation and cytokine secretion in an RBP-J (and thus, Notch) independent manner. The controversies surrounding the role of Notch and presenilins in Th1/Th2 polarization may reflect their role as genetic modifiers of T-helper cells differentiation