SAGE: Sequential Attribute Generator for Analyzing Glioblastomas using Limited Dataset

While deep learning approaches have shown remarkable performance in many imaging tasks, most of these methods rely on availability of large quantities of data. Medical image data, however, is scarce and fragmented. Generative Adversarial Networks (GANs) have recently been very effective in handling such datasets by generating more data. If the datasets are very small, however, GANs cannot learn the data distribution properly, resulting in less diverse or low-quality results. One such limited dataset is that for the concurrent gain of 19 and 20 chromosomes (19/20 co-gain), a mutation with positive prognostic value in Glioblastomas (GBM). In this paper, we detect imaging biomarkers for the mutation to streamline the extensive and invasive prognosis pipeline. Since this mutation is relatively rare, i.e. small dataset, we propose a novel generative framework - the Sequential Attribute GEnerator (SAGE), that generates detailed tumor imaging features while learning from a limited dataset. Experiments show that not only does SAGE generate high quality tumors when compared to standard Deep Convolutional GAN (DC-GAN) and Wasserstein GAN with Gradient Penalty (WGAN-GP), it also captures the imaging biomarkers accurately

Eicosanoids and Respiratory Viral Infection: Coordinators of Inflammation and Potential Therapeutic Targets

Viruses are frequent causes of respiratory infection, and viral respiratory infections are significant causes of hospitalization, morbidity, and sometimes mortality in a variety of patient populations. Lung inflammation induced by infection with common respiratory pathogens such as influenza and respiratory syncytial virus is accompanied by increased lung production of prostaglandins and leukotrienes, lipid mediators with a wide range of effects on host immune function. Deficiency or pharmacologic inhibition of prostaglandin and leukotriene production often results in a dampened inflammatory response to acute infection with a respiratory virus. These mediators may, therefore, serve as appealing therapeutic targets for disease caused by respiratory viral infection

A Budget and Accounting of Metals at z~0: Results from the COS-Halos Survey

We present a budget and accounting of metals in and around star-forming galaxies at $z\sim 0$. We combine empirically derived star formation histories with updated supernova and AGB yields and rates to estimate the total mass of metals produced by galaxies with present-day stellar mass of $10^{9.3}$--$10^{11.6} M_{\odot}$. On the accounting side of the ledger, we show that a surprisingly constant 20--25% mass fraction of produced metals remain in galaxies' stars, interstellar gas and interstellar dust, with little dependence of this fraction on the galaxy stellar mass (omitting those metals immediately locked up in remnants). Thus, the bulk of metals are outside of galaxies, produced in the progenitors of today's $L^*$ galaxies. The COS-Halos survey is uniquely able to measure the mass of metals in the circumgalactic medium (to impact parameters of $< 150$ kpc) of low-redshift $\sim L^*$ galaxies. Using these data, we map the distribution of CGM metals as traced by both the highly ionized OVI ion and a suite of low-ionization species; combined with constraints on circumgalactic dust and hotter X-ray emitting gas out to similar impact parameters, we show that $\sim 40$% of metals produced by $M_{\star}\sim 10^{10}M_{\odot}$ galaxies can be easily accounted for out to 150 kpc. With the current data, we cannot rule out a constant mass of metals within this fixed physical radius. This census provides a crucial boundary condition for the eventual fate of metals in galaxy evolution models.Comment: 19 pages, 12 figures, 2 tables. ApJ, in pres

Gammaherpesvirus modulation of mouse adenovirus type 1 pathogenesis

AbstractImmune function is likely to be shaped by multiple infections over time. Infection with one pathogen can confer cross-protection against heterologous pathogens. We tested the hypothesis that latent murine gammaherpesvirus 68 (γHV68) infection modulates host inflammatory responses and susceptibility to mouse adenovirus type 1 (MAV-1). Mice were infected intranasally (i.n.) with γHV68. 21 days later, they were infected i.n. with MAV-1. We assessed cytokine and chemokine expression by quantitative reverse transcriptase real-time PCR, cellular inflammation by histology, and viral loads by quantitative real-time PCR. Previous γHV68 infection led to persistently upregulated IFN-γ in lungs and spleen and persistently upregulated CCL2 and CCL5 in the lungs. Previous γHV68 infection amplified MAV-1-induced CCL5 upregulation and cellular inflammation in the lungs. Previous γHV68 infection was associated with lower MAV-1 viral loads in the spleen but not the lung. There was no significant effect of previous γHV68 on IFN-γ expression or MAV-1 viral loads when the interval between infections was increased to 44 days. In summary, previous γHV68 infection modulated lung inflammatory responses and decreased susceptibility to a heterologous virus in an organ- and time-dependent manner

Gut Dysbiosis Promotes M2 Macrophage Polarization and Allergic Airway Inflammation via Fungi-Induced PGE2

SummaryAlthough imbalances in gut microbiota composition, or “dysbiosis,” are associated with many diseases, the effects of gut dysbiosis on host systemic physiology are less well characterized. We report that gut dysbiosis induced by antibiotic (Abx) treatment promotes allergic airway inflammation by shifting macrophage polarization in the lung toward the alternatively activated M2 phenotype. Adoptive transfer of alveolar macrophages derived from Abx-treated mice was sufficient to increase allergic airway inflammation. Abx treatment resulted in the overgrowth of a commensal fungal Candida species in the gut and increased plasma concentrations of prostaglandin E2 (PGE2), which induced M2 macrophage polarization in the lung. Suppression of PGE2 synthesis by the cyclooxygenase inhibitors aspirin and celecoxib suppressed M2 macrophage polarization and decreased allergic airway inflammatory cell infiltration in Abx-treated mice. Thus, Abx treatment can cause overgrowth of particular fungal species in the gut and promote M2 macrophage activation at distant sites to influence systemic responses including allergic inflammation