Harmonically Trapped Quantum Gases

We solve the problem of a Bose or Fermi gas in $d$-dimensions trapped by $\delta \leq d$ mutually perpendicular harmonic oscillator potentials. From the grand potential we derive their thermodynamic functions (internal energy, specific heat, etc.) as well as a generalized density of states. The Bose gas exhibits Bose-Einstein condensation at a nonzero critical temperature $T_{c}$ if and only if $d+\delta >2$, and a jump in the specific heat at $T_{c}$ if and only if $d+\delta >4$. Specific heats for both gas types precisely coincide as functions of temperature when $d+\delta =2$. The trapped system behaves like an ideal free quantum gas in $d+\delta$ dimensions. For $\delta =0$ we recover all known thermodynamic properties of ideal quantum gases in $d$ dimensions, while in 3D for $\delta =$ 1, 2 and 3 one simulates behavior reminiscent of quantum {\it wells, wires}and{\it dots}, respectively.Comment: 14 pages including 3 figures and 3 table

Multi-connected Momentum Distribution and Fermion Condensation

The structure of the ground state beyond the instability point of the quasiparticle system with Fermi-step momentum distribution is studied within the model of a Fermi liquid with a strong repulsive interaction. A ground state rearrangement occurs as the interaction strength is increased beyond a definite critical value. Numerical investigation of the initial stage of this structural transition shows that there are two temperature regions, corresponding to different scenarios of the rearrangement. While for temperature T larger than some characteristic temperature T_0 the behaviour of the system is the same as that in the case of the fermion condensation, for T<T_0 the intermediate structure with multi-connected quasiparticle momentum distribution arises. The transition of this structure to the fermion condensate at increasing interaction strength is discussed.Comment: 10 pages, 8 postscript figure

Is asthma control more than just an absence of symptoms? An expert consensus statement

Purpose: Definitions and measures of asthma control used in clinical trials and in clinical practice vary considerably. There is also misalignment between patients and healthcare professionals (HCPs) in terms of understanding and managing asthma control. This study aimed to progress towards a consensus definition of asthma control, and evaluate disparities between HCP and patient perspectives. Basic procedures: A two-stage Delphi questionnaire involving asthma specialists sought to identify areas of consensus on aspects of asthma control in clinical practice. Results were compared with those of a structured literature review to assess if existing guidance and measures of asthma control used in studies correlated with practice. Eighty-two panelists took part in the Delphi questionnaire. The structured literature review included 185 manuscripts and 31 abstracts. Main findings: Panelists agreed that there was no standard definition of asthma control, confirmed by a total of 19 different composite consensus/guideline definitions and/or validated measures of control being identified across the Delphi study and literature review. Panelists agreed on the positive associations of well-controlled asthma with patient outcomes, but not on the components or thresholds of a working definition of control. Principal conclusions: A universally accepted definition and measure of asthma control that is utilized and understood by patients, HCPs, and researchers is required

Cooper pair dispersion relation for weak to strong coupling

Cooper pairing in two dimensions is analyzed with a set of renormalized equations to determine its binding energy for any fermion number density and all coupling assuming a generic pairwise residual interfermion interaction. \ Also considered are Cooper pairs (CPs) with nonzero center-of-mass momentum (CMM)--usually neglected in BCS theory--and their binding energy is expanded analytically in powers of the CMM up to quadratic terms. A Fermi-sea-dependent {\it linear} term in the CMM dominates the pair excitation energy in weak coupling (also called the BCS regime) while the more familiar quadratic term prevails in strong coupling (the Bose regime). The crossover, though strictly unrelated to BCS theory {\it per se,} is studied numerically as it is expected to play a central role in a model of superconductivity as a Bose-Einstein condensation of CPs where the transition temperature vanishes for all dimensionality $d\leq 2$ for quadratic dispersion, but is {\it nonzero} for all $d\geq 1$ for linear dispersion.Comment: 11 pages plus 3 figures, revised version accepted in Physical Review

LEDGF/p75 Proteins with Alternative Chromatin Tethers Are Functional HIV-1 Cofactors

LEDGF/p75 can tether over-expressed lentiviral integrase proteins to chromatin but how this underlies its integration cofactor role for these retroviruses is unclear. While a single integrase binding domain (IBD) binds integrase, a complex N-terminal domain ensemble (NDE) interacts with unknown chromatin ligands. Whether integration requires chromatin tethering per se, specific NDE-chromatin ligand interactions or other emergent properties of LEDGF/p75 has been elusive. Here we replaced the NDE with strongly divergent chromatin-binding modules. The chimeras rescued integrase tethering and HIV-1 integration in LEDGF/p75-deficient cells. Furthermore, chromatin ligands could reside inside or outside the nucleosome core, and could be protein or DNA. Remarkably, a short Kaposi's sarcoma virus peptide that binds the histone 2A/B dimer converted GFP-IBD from an integration blocker to an integration cofactor that rescues over two logs of infectivity. NDE mutants were corroborative. Chromatin tethering per se is a basic HIV-1 requirement and this rather than engagement of particular chromatin ligands is important for the LEDGF/p75 cofactor mechanism

Bose-Einstein condensation in multilayers

The critical BEC temperature $T_{c}$ of a non interacting boson gas in a layered structure like those of cuprate superconductors is shown to have a minimum $T_{c,m}$, at a characteristic separation between planes $a_{m}$. It is shown that for $a<a_{m}$, $T_{c}$ increases monotonically back up to the ideal Bose gas $T_{0}$ suggesting that a reduction in the separation between planes, as happens when one increases the pressure in a cuprate, leads to an increase in the critical temperature. For finite plane separation and penetrability the specific heat as a function of temperature shows two novel crests connected by a ridge in addition to the well-known BEC peak at $T_{c}$ associated with the 3D behavior of the gas. For completely impenetrable planes the model reduces to many disconnected infinite slabs for which just one hump survives becoming a peak only when the slab widths are infinite.Comment: Four pages, four figure

Accelerated in vivo proliferation of memory phenotype CD4+ T-cells in human HIV-1 infection irrespective of viral chemokine co-receptor tropism.

CD4(+) T-cell loss is the hallmark of HIV-1 infection. CD4 counts fall more rapidly in advanced disease when CCR5-tropic viral strains tend to be replaced by X4-tropic viruses. We hypothesized: (i) that the early dominance of CCR5-tropic viruses results from faster turnover rates of CCR5(+) cells, and (ii) that X4-tropic strains exert greater pathogenicity by preferentially increasing turnover rates within the CXCR4(+) compartment. To test these hypotheses we measured in vivo turnover rates of CD4(+) T-cell subpopulations sorted by chemokine receptor expression, using in vivo deuterium-glucose labeling. Deuterium enrichment was modeled to derive in vivo proliferation (p) and disappearance (d*) rates which were related to viral tropism data. 13 healthy controls and 13 treatment-naive HIV-1-infected subjects (CD4 143-569 cells/ul) participated. CCR5-expression defined a CD4(+) subpopulation of predominantly CD45R0(+) memory cells with accelerated in vivo proliferation (p = 2.50 vs 1.60%/d, CCR5(+) vs CCR5(-); healthy controls; P<0.01). Conversely, CXCR4 expression defined CD4(+) T-cells (predominantly CD45RA(+) naive cells) with low turnover rates. The dominant effect of HIV infection was accelerated turnover of CCR5(+)CD45R0(+)CD4(+) memory T-cells (p = 5.16 vs 2.50%/d, HIV vs controls; P<0.05), naïve cells being relatively unaffected. Similar patterns were observed whether the dominant circulating HIV-1 strain was R5-tropic (n = 9) or X4-tropic (n = 4). Although numbers were small, X4-tropic viruses did not appear to specifically drive turnover of CXCR4-expressing cells (p = 0.54 vs 0.72 vs 0.44%/d in control, R5-tropic, and X4-tropic groups respectively). Our data are most consistent with models in which CD4(+) T-cell loss is primarily driven by non-specific immune activation