Paths to Understanding Birational Rowmotion on Products of Two Chains

Birational rowmotion is an action on the space of assignments of rational functions to the elements of a finite partially-ordered set (poset). It is lifted from the well-studied rowmotion map on order ideals (equivariantly on antichains) of a poset $P$, which when iterated on special posets, has unexpectedly nice properties in terms of periodicity, cyclic sieving, and homomesy (statistics whose averages over each orbit are constant) [AST11, BW74, CF95, Pan09, PR13, RuSh12,RuWa15+,SW12, ThWi17, Yil17. In this context, rowmotion appears to be related to Auslander-Reiten translation on certain quivers, and birational rowmotion to $Y$-systems of type $A_m \times A_n$ described in Zamolodchikov periodicity. We give a formula in terms of families of non-intersecting lattice paths for iterated actions of the birational rowmotion map on a product of two chains. This allows us to give a much simpler direct proof of the key fact that the period of this map on a product of chains of lengths $r$ and $s$ is $r+s+2$ (first proved by D.~Grinberg and the second author), as well as the first proof of the birational analogue of homomesy along files for such posets.Comment: 31 pages, to appear in Algebraic Combinatoric

Characterization of the defective interaction between a subset of natural killer cells and dendritic cells in HIV-1 infection

In this study, we demonstrate that the in vitro interactions between a CD56neg/CD16pos (CD56neg) subset of natural killer (NK) cells and autologous dendritic cells (DCs) from HIV-1–infected viremic but not aviremic individuals are markedly impaired and likely interfere with the development of an effective immune response. Among the defective interactions are abnormalities in the process of reciprocal NK–DC activation and maturation as well as a defect in the NK cell–mediated editing or elimination of immature DCs (iDCs). Notably, the lysis of mature DCs (mDCs) by autologous NK cells was highly impaired even after the complete masking of major histocompatibility complex I molecules, suggesting that the defective elimination of autologous iDCs is at the level of activating NK cell receptors. In this regard, the markedly impaired expression/secretion and function of NKp30 and TNF-related apoptosis-inducing ligand, particularly among the CD56neg NK cell subset, largely accounts for the highly defective NK cell–mediated lysis of autologous iDCs. Moreover, mDCs generated from HIV-1 viremic but not aviremic patients are substantially impaired in their ability to secrete interleukin (IL)-10 and -12 and to prime the proliferation of neighboring autologous NK cells, which, in turn, fail to secrete adequate amounts of interferon-γ

The chemical abundance analysis of normal early A- and late B-type stars

Modern spectroscopy of early-type stars often aims at studying complex physical phenomena. Comparatively less attention is paid to identifying and studying the "normal" A- and B-type stars and testing how the basic atomic parameters and standard spectral analysis allow one to fit the observations. We wish to stablish whether the chemical composition of the solar photosphere can be regarded as a reference for early A- and late B-type stars. We have obtained optical high-resolution, high signal-to-noise ratio spectra of three slowly rotating early-type stars (HD 145788, 21 Peg and pi Cet) that show no obvious sign of chemical peculiarity, and performed a very accurate LTE abundance analysis of up to 38 ions of 26 elements (for 21 Peg), using a vast amount of spectral lines visible in the spectral region covered by our spectra. We provide an exhaustive description of the abundance characteristics of the three analysed stars with a critical review of the line parameters used to derive the abundances. We compiled a table of atomic data for more than 1100 measured lines that may be used in the future as a reference. The abundances we obtained for He, C, Al, S, V, Cr, Mn, Fe, Ni, Sr, Y, and Zr are compatible with the solar ones derived with recent 3D radiative-hydrodynamical simulations of the solar photosphere. The abundances of the remaining studied elements show some degree of discrepancy compared to the solar photosphere. Those of N, Na, Mg, Si, Ca, Ti, and Nd may well be ascribed to non-LTE effects; for P, Cl, Sc and Co, non-LTE effects are totally unknown; O, Ne, Ar, and Ba show discrepancies that cannot be ascribed to non-LTE effects. The discrepancies obtained for O (in two stars) and Ne agree with very recent non-LTE abundance analysis of early B-type stars in the solar neighbourhood.Comment: Accepted for publication on Astronomy and Astrophysic

LSST: from Science Drivers to Reference Design and Anticipated Data Products

(Abridged) We describe here the most ambitious survey currently planned in the optical, the Large Synoptic Survey Telescope (LSST). A vast array of science will be enabled by a single wide-deep-fast sky survey, and LSST will have unique survey capability in the faint time domain. The LSST design is driven by four main science themes: probing dark energy and dark matter, taking an inventory of the Solar System, exploring the transient optical sky, and mapping the Milky Way. LSST will be a wide-field ground-based system sited at Cerro Pach\'{o}n in northern Chile. The telescope will have an 8.4 m (6.5 m effective) primary mirror, a 9.6 deg$^2$ field of view, and a 3.2 Gigapixel camera. The standard observing sequence will consist of pairs of 15-second exposures in a given field, with two such visits in each pointing in a given night. With these repeats, the LSST system is capable of imaging about 10,000 square degrees of sky in a single filter in three nights. The typical 5$\sigma$ point-source depth in a single visit in $r$ will be $\sim 24.5$ (AB). The project is in the construction phase and will begin regular survey operations by 2022. The survey area will be contained within 30,000 deg$^2$ with $\delta<+34.5^\circ$, and will be imaged multiple times in six bands, $ugrizy$, covering the wavelength range 320--1050 nm. About 90\% of the observing time will be devoted to a deep-wide-fast survey mode which will uniformly observe a 18,000 deg$^2$ region about 800 times (summed over all six bands) during the anticipated 10 years of operations, and yield a coadded map to $r\sim27.5$. The remaining 10\% of the observing time will be allocated to projects such as a Very Deep and Fast time domain survey. The goal is to make LSST data products, including a relational database of about 32 trillion observations of 40 billion objects, available to the public and scientists around the world.Comment: 57 pages, 32 color figures, version with high-resolution figures available from https://www.lsst.org/overvie

Impact of HIV on Cell Survival and Antiviral Activity of Plasmacytoid Dendritic Cells

Plasmacytoid dendritic cells (pDCs) are important mediators of innate immunity that act mainly through secretion of interferon (IFN)-α. Previous studies have found that these cells can suppress HIV in vitro; additionally, pDCs have been shown to be severely reduced in the peripheral blood of HIV-infected individuals. In the present study, we sought to determine the ability of pDCs to directly suppress viral replication ex vivo and to delineate the potential mechanisms whereby pDCs are depleted in HIV-infected individuals. We demonstrate that activated pDCs strongly suppress HIV replication in autologous CD4(+) T cells via a mechanism involving IFN-α as well as other antiviral factors. Of note, unstimulated pDCs from infected individuals who maintain low levels of plasma viremia without antiretroviral therapy were able to suppress HIV ex vivo via a mechanism requiring cell-to-cell contact. Our data also demonstrate that death of pDCs by both apoptosis and necrosis is induced by fusion of HIV with pDCs. Taken together, our data suggest that pDCs play an important role in the control of HIV replication and that high levels of viral replication in vivo are associated with pDC cell death via apoptosis and necrosis. Elucidation of the mechanism by which pDCs suppress HIV replication in vivo may have clinically relevant implications for future therapeutic strategies

Suppression of HIV-specific T cell activity by lymph node CD25+ regulatory T cells from HIV-infected individuals

CD25(+) CD4(+) FoxP3(+) regulatory T (Treg) cells isolated from the peripheral blood of asymptomatic HIV-infected individuals have been demonstrated to significantly suppress HIV-specific immune responses in vitro. CD25(+) Treg cell suppressor activity in the peripheral blood seems to diminish with progression of HIV disease, and it has been suggested that loss of Treg cells contributes to aberrant immune activation and disease progression. However, phenotypic studies suggest that Treg cells may migrate to, and be maintained or even expanded in, tissue sites of HIV replication. Currently, it is not known whether tissue-associated Treg cells maintain suppressive activity in the context of HIV infection, particularly in individuals with advanced disease. The present study demonstrates that CD25(+) Treg cells isolated from lymph nodes and peripheral blood of HIV(+) subjects, even those with high viral loads and/or low CD4(+) T cell counts, maintain potent suppressive activity against HIV-specific cytolytic T cell function. This activity was better in lymph node as compared with peripheral blood, particularly in patients with high levels of plasma viremia. In addition, the expression of certain CD25(+) Treg-associated markers on CD4(+) T cells isolated from lymph nodes differed significantly from those on CD4(+) T cell subsets isolated from the peripheral blood. These data suggest that CD25(+) Treg cell-mediated suppression of HIV-specific responses continues throughout the course of HIV disease and, because of their particularly potent suppression of HIV-specific CTL activity in lymphoid tissue, may considerably impact the ability to control HIV replication in vivo

Could Human Papillomaviruses Be Spread through Blood?

The human papillomaviruses (HPVs) are epitheliotropic viruses that require the environment of a differentiating squamous epithelium for their life cycle. HPV infection through abrasion of the skin or sexual intercourse causes benign warts and sometimes cancer. HPV DNA detected in the blood has been interpreted as having originated from metastasized cancer cells. The present study examined HPV DNA in banked, frozen peripheral blood mononuclear cells (PBMCs) from 57 U.S. human immunodeficiency virus (HIV)-infected pediatric patients collected between 1987 and 1996 and in fresh PBMCs from 19 healthy blood donors collected in 2002 to 2003. Eight patients and three blood donors were positive mostly for two subgroups of the HPV type 16 genome. The HPV genome detected in all 11 PBMC samples existed as an episomal form, albeit at a low DNA copy number. Among the eight patients, seven acquired HIV from transfusion (three associated with hemophilia) and one acquired HIV through vertical transmission; this patient also had received a transfusion before sampling. Our data suggest that PBMCs may be HPV carriers and might spread the virus through blood