A Study of the Comparative Effects of Titanium Dioxide on Paper Brightness and Opacity When Used as Filler versus Its Use as a Coating Mineral

Introduction Because of the fact, that advertisements printed on bright papers have the most appeal, and papers printed on both sides must have absence of show-through, brightness and opacity have become important variables in paper making. Titanium dioxide used a a filler or as a coating mineral will cause an increase in paper opacity and brightness. Because titanium dioxide is expensive, it is important to know how it can be used (as filler or coating) to the best advantage. Objective The purpose of this project is to compare the optical gains (opacity and brightness) imparted to paper by using titanium dioxide as a filler versus its use as a coating mineral

Infrastructure for 3D model reconstruction of marine structures

3D model reconstruction of marine structures, such as dams, oil-rigs, and sea caves, is both important and challenging. An important application includes structural inspection. Manual inspection of marine structures is tedious and even a small oversight can have severe consequences for the structure and the people around it. A robotic system that can construct 3D models of marine structures would hopefully reduce the chances of oversight, and hence improve the safety of marine environment. Due to the water currents and wakes, developing a robotic system to construct 3D models of marine structures is a challenge, as it is difficult for a robot to reach the desired scan configurations and take a scan of the environment while remaining stationary. This paper presents our preliminary work in developing a robotic and software system for construction of 3D models of marine structures. We have successfully tested our system in a sea water environment in the Singapore Straits

Rocaglates as dual-targeting agents for experimental cerebral malaria

Cerebral malaria (CM) is a severe and rapidly progressing complication of infection by Plasmodium parasites that is associated with high rates of mortality and morbidity. Treatment options are currently few, and intervention with artemisinin (Art) has limited efficacy, a problem that is compounded by the emergence of resistance to Art in Plasmodium parasites. Rocaglates are a class of natural products derived from plants of the Aglaia genus that have been shown to interfere with eukaryotic initiation factor 4A (eIF4A), ultimately blocking initiation of protein synthesis. Here, we show that the rocaglate CR-1-31B perturbs association of Plasmodium falciparum eIF4A (PfeIF4A) with RNA. CR-1-31B shows potent prophylactic and therapeutic antiplasmodial activity in vivo in mouse models of infection with Plasmodium berghei (CM) and Plasmodium chabaudi (blood-stage malaria), and can also block replication of different clinical isolates of P. falciparum in human erythrocytes infected ex vivo, including drug-resistant P. falciparum isolates. In vivo, a single dosing of CR-1-31B in P. berghei-infected animals is sufficient to provide protection against lethality. CR-1-31B is shown to dampen expression of the early proinflammatory response in myeloid cells in vitro and dampens the inflammatory response in vivo in P. berghei-infected mice. The dual activity of CR-1-31B as an antiplasmodial and as an inhibitor of the inflammatory response in myeloid cells should prove extremely valuable for therapeutic intervention in human cases of CM.We thank Susan Gauthier, Genevieve Perreault, and Patrick Senechal for technical assistance. This work was supported by a research grant (to P.G.) from the Canadian Institutes of Health Research (CIHR) (Foundation Grant). J.P. and P.G. are supported by a James McGill Professorship salary award. D.L. is supported by fellowships from the Fonds de recherche sante Quebec, the CIHR Neuroinflammation training program. J.P. is supported by CIHR Research Grant FDN-148366. M.S. is supported by a CIHR Foundation grant. J.A.P. is supported by NIH Grant R35 GM118173. Work at the Boston University Center for Molecular Discovery is supported by Grant R24 GM111625. K.C.K. was supported by a CIHR Foundation Grant and the Canada Research Chair program. (Canadian Institutes of Health Research (CIHR); James McGill Professorship salary award; Fonds de recherche sante Quebec; CIHR Neuroinflammation training program; FDN-148366 - CIHR Research Grant; CIHR Foundation grant; R35 GM118173 - NIH; Canada Research Chair program; R24 GM111625

Nuclear factor I coordinates multiple phases of cerebellar granule cell development via regulation of cell adhesion molecules

A central question is how various stages of neuronal development are integrated as a differentiation program. Here we show that the nuclear factor I (NFI) family of transcriptional regulators is expressed and functions throughout the postmitotic development of cerebellar granule neurons (CGNs). Expression of an NFI dominant repressor in CGN cultures blocked axon outgrowth and dendrite formation and decreased CGN migration. Inhibition of NFI transactivation also disrupted extension and fasciculation of parallel fibers as well as CGN migration to the internal granule cell layer in cerebellar slices. In postnatal day 17 Nfia-deficient mice, parallel fibers were greatly diminished and disoriented, CGN dendrite formation was dramatically impaired, and migration from the external germinal layer (EGL) was retarded. Axonal marker expression also was disrupted within the EGL of embryonic day 18 Nfib-null mice. NFI regulation of axon extension was observed under conditions of homotypic cell contact, implicating cell surface proteins as downstream mediators of its actions in CGNs. Consistent with this, the cell adhesion molecules ephrin B1 and N-cadherin were identified as NFI gene targets in CGNs using inhibitor and Nfi mutant analysis as well as chromatin immunoprecipitation. Functional inhibition of ephrin B1 or N-cadherin interfered with CGN axon extension and guidance, migration, and dendritogenesis in cell culture as well as in situ. These studies define NFI as a key regulator of postmitotic CGN development, in particular of axon formation, dendritogenesis, and migratory behavior. Furthermore, they reveal how a single transcription factor family can control and integrate multiple aspects of neuronal differentiation through the regulation of cell adhesion molecules

Contextualizing our Leadership Education Approach to Complex Problem Solving: Shifting Paradigms and Evolving Knowledge: Priority 5 of the National Leadership Education Research Agenda 2020–2025

Complex problems characterized by uncertainty, interconnectedness, poorly defined goals, and high risk are not new to the human experience. Yet humanity is increasingly faced with multifaceted and pervasive global challenges, and leadership education must adapt accordingly. These complex problems transcend borders and require a collective, adaptive, and iterative learning response. Complex problems such as failure to act on climate change, unemployment, food crises, governance failures, pandemics, cyberattacks, and involuntary migration are interrelated challenges that require paradigm shifts in responses and leadership (Global Risk Report, 2020)

Dopamine receptor activation modulates GABA neuron migration from the basal forebrain to the cerebral cortex

GABA neurons of the cerebral cortex and other telencephalic structures are produced in the basal forebrain and migrate to their final destinations during the embryonic period. The embryonic basal forebrain is enriched in dopamine and its receptors, creating a favorable environment for dopamine to influence GABA neuron migration. However, whether dopamine receptor activation can influence GABA neuron migration is not known. We show that dopamine D1 receptor activation promotes and D2 receptor activation decreases GABA neuron migration from the medial and caudal ganglionic eminences to the cerebral cortex in slice preparations of embryonic mouse forebrain. Slice preparations from D1 or D2 receptor knock-out mouse embryos confirm the findings. In addition, D1 receptor electroporation into cells of the basal forebrain and pharmacological activation of the receptor promote migration of the electroporated cells to the cerebral cortex. Analysis of GABA neuron numbers in the cerebral wall of the dopamine receptor knock-out mouse embryos further confirmed the effects of dopamine receptor activation on GABA neuron migration. Finally, dopamine receptor activation mobilizes striatal neuronal cytoskeleton in a manner consistent with the effects on neuronal migration. These data show that impairing the physiological balance between D1 and D2 receptors can alter GABA neuron migration from the basal forebrain to the cerebral cortex. The intimate relationship between dopamine and GABA neuron development revealed here may offer novel insights into developmental disorders such as schizophrenia, attention deficit or autism, and fetal cocaine exposure, all of which are associated with dopamine and GABA imbalance

Mesoscopic structure and social aspects of human mobility

The individual movements of large numbers of people are important in many contexts, from urban planning to disease spreading. Datasets that capture human mobility are now available and many interesting features have been discovered, including the ultra-slow spatial growth of individual mobility. However, the detailed substructures and spatiotemporal flows of mobility - the sets and sequences of visited locations - have not been well studied. We show that individual mobility is dominated by small groups of frequently visited, dynamically close locations, forming primary "habitats" capturing typical daily activity, along with subsidiary habitats representing additional travel. These habitats do not correspond to typical contexts such as home or work. The temporal evolution of mobility within habitats, which constitutes most motion, is universal across habitats and exhibits scaling patterns both distinct from all previous observations and unpredicted by current models. The delay to enter subsidiary habitats is a primary factor in the spatiotemporal growth of human travel. Interestingly, habitats correlate with non-mobility dynamics such as communication activity, implying that habitats may influence processes such as information spreading and revealing new connections between human mobility and social networks.Comment: 7 pages, 5 figures (main text); 11 pages, 9 figures, 1 table (supporting information

The propagator for the step potential and delta function potential using the path decomposition expansion

We present a derivation of the propagator for a particle in the presence of the step and delta function potentials. These propagators are known, but we present a direct path integral derivation, based on the path decomposition expansion and the Brownian motion definition of the path integral. The derivation exploits properties of the Catalan numbers, which enumerate certain classes of lattice paths.Comment: 11 pages, 3 figure

The Ursinus Weekly, October 5, 1972

Jerrold Schecter speaks on China: Mao in control • Ursinus administration appoints twelve new faculty members for coming year • Voting deadline nears; Have you registered? • News editors hope for expansion and diversity • Editorial: A falling star? • Focus: Andrea Turner • Ursinus receives a big fat government grant • Coordinating the freshmen, or Thank God for the relay races • Tired of classes? • Harriers upset by DelVal; Win streak ends • Soccer team impressive in Villanova victory • New coach takes over • Gridders drop first two to F&M, Lebanon Valley • Sports buffs\u27 corner • Sports scoreboardhttps://digitalcommons.ursinus.edu/weekly/1086/thumbnail.jp

Gene Expression Changes Associated with Resistance to Intravenous Corticosteroid Therapy in Children with Severe Ulcerative Colitis

Microarray analysis of RNA expression allows gross examination of pathways operative in inflammation. We aimed to determine whether genes expressed in whole blood early following initiation of intravenous corticosteroid treatment can be associated with response.From a prospectively accrued cohort of 128 pediatric patients hospitalized for intravenous corticosteroid treatment of severe UC, we selected for analysis 20 corticosteroid responsive (hospital discharge or PUCAI ≤45 by day 5) and 20 corticosteroid resistant patients (need for second line medical therapy or colectomy, or PUCAI >45 by day 5). Total RNA was extracted from blood samples collected on day 3 of intravenous corticosteroid therapy. The eluted transcriptomes were quantified on Affymetrix Human Gene 1.0 ST arrays. The data was analysed by the local-pooled error method for discovery of differential gene expression and false discovery rate correction was applied to adjust for multiple comparisons.A total of 41 genes differentially expressed between responders and non-responders were detected with statistical significance. Two of these genes, CEACAM1 and MMP8, possibly inhibited by methylprednisolone through IL8, were both found to be over-expressed in non-responsive patients. ABCC4 (MRP4) as a member of the multi-drug resistance superfamily was a novel candidate gene for corticosteroid resistance. The expression pattern of a cluster of 10 genes selected from the 41 significant hits were able to classify the patients with 80% sensitivity and 80% specificity.Elevated expression of several genes involved in inflammatory pathways was associated with resistance to intravenous corticosteroid therapy early in the course of treatment. Gene expression profiles may be useful to classify resistance to intravenous corticosteroids in children with severe UC and assist with clinical management decisions