An AI approach for scheduling space-station payloads at Kennedy Space Center

The Payload Processing for Space-Station Operations (PHITS) is a prototype modeling tool capable of addressing many Space Station related concerns. The system's object oriented design approach coupled with a powerful user interface provide the user with capabilities to easily define and model many applications. PHITS differs from many artificial intelligence based systems in that it couples scheduling and goal-directed simulation to ensure that on-orbit requirement dates are satisfied

The Ursinus Weekly, May 19, 1941

Meeting post to direct grads on Alumni Day • Plans near completion for graduation weekend activities, June 6,7,8, and 9 • Invitation to revolution is vespers\u27 challenge • Tyson to address bear athletes at Varsity Club dinner • Woody Leh and orchestra syncopate for May hop • Debaters hold joint banquet at close of year\u27s activity • Waltz dream by Straus is commencement operetta • Morris\u27 varied program scores big success as his valedictory concert • Y prexies announce cabinets for next year • Students in science look forward to work in graduate schools • Final examination: Second semester 1941 • Britannica cites Dr. Price as authority on common colds • Baseballers win four straight; defeat Juniata Friday 4-1 • Cindermen hit stride and defeat Lions in close meet Saturday; Hartzell stars • Co-eds defeat Temple and Rhode Island, 5-0 • Baker wicketmen defeat Penn but lose to Princeton 35-20 • Slotter fans 18 as Perkiomen preppers stop jay-vees 9-6 • Women golfers lose to Beaverhttps://digitalcommons.ursinus.edu/weekly/1819/thumbnail.jp

The Ursinus Weekly, December 15, 1941

Students to enjoy festive board and banquet addresses • Capacity audience Thursday evening hears fourth rendition of Messiah • Pre-meds will hear Winkleman, neurologist, at meeting tomorrow • Y Christmas basket drive nets $31.25 for Red Cross • Men debaters hold informal meeting at Dr. Carter\u27s home • Inclement weather fails to dampen exuberance of gay senior weekend • Wednesday Xmas party will present a sultan, his court, and dancing • Dr. Lentz to serve holy elements at service Thursday • Fred Waring\u27s Pennsylvanians promise to do song for Ursinus • Winner of national forensic contest to receive$1,000 • Dr. Kohman tells of nutritional value of canned foods • Frosh women debaters to engage high school on issue of the draft • French Club to be sponsor of Mayerling on January 9 • Bear grapplers down Kutztown foe by 20-16 score in season\u27s opening meet • Hockey squad compiles enviable record of five wins against single loss • Engineers\u27 third quarter scoring sinks bears, 53-37 • Regional trainers honor bears trainer Jim Tadleyhttps://digitalcommons.ursinus.edu/weekly/1773/thumbnail.jp

The Ursinus Weekly, December 1, 1941

Prince Zu Loewenstein, German exile, will speak at first forum Wednesday • Handel\u27s Messiah to open Christmas season at Ursinus • Artists to present viola-piano recital here Wednesday • \u27Know your Money\u27 is title of G-man movie Wednesday • Opening of Ye olde bear tavern will be feature of weekend party • Current labor problem is topic of confab as women debaters meet • Contralto and baritone soloists boast background of experience • Seven from Ursinus attend IRC conference at Lehigh • Over fifty attain special renown as Dean\u27s list makes its debut • Inspired bears downed by Diplomats 14-13 in thrilling game Thursday • William Power \u2739 to coach frosh basketball team • Hashagen drills court squad for opener against Lehigh • Miss Snell heads clinic for basketball coaches and players of regionhttps://digitalcommons.ursinus.edu/weekly/1771/thumbnail.jp

Loss of the Desmosomal Component Perp Impairs Wound Healing In Vivo

Epithelial wound closure is a complex biological process that relies on the concerted action of activated keratinocytes and dermal fibroblasts to resurface and close the exposed wound. Modulation of cell-cell adhesion junctions is thought to facilitate cellular proliferation and migration of keratinocytes across the wound. In particular, desmosomes, adhesion complexes critical for maintaining epithelial integrity, are downregulated at the wound edge. It is unclear, however, how compromised desmosomal adhesion would affect wound reepithelialization, given the need for a delicate balance between downmodulating adhesive strength to permit changes in cellular morphology and maintaining adhesion to allow coordinated migration of keratinocyte sheets. Here, we explore the contribution of desmosomal adhesion to wound healing using mice deficient for the desmosomal component Perp. We find that Perp conditional knockout mice display delayed wound healing relative to controls. Furthermore, we determine that while loss of Perp compromises cell-cell adhesion, it does not impair keratinocyte proliferation and actually enhances keratinocyte migration in in vitro assays. Thus, Perp's role in promoting cell adhesion is essential for wound closure. Together, these studies suggest a role for desmosomal adhesion in efficient wound healing

Developmental Context Determines Latency of MYC-Induced Tumorigenesis

One of the enigmas in tumor biology is that different types of cancers are prevalent in different age groups. One possible explanation is that the ability of a specific oncogene to cause tumorigenesis in a particular cell type depends on epigenetic parameters such as the developmental context. To address this hypothesis, we have used the tetracycline regulatory system to generate transgenic mice in which the expression of a c-MYC human transgene can be conditionally regulated in murine hepatocytes. MYC's ability to induce tumorigenesis was dependent upon developmental context. In embryonic and neonatal mice, MYC overexpression in the liver induced marked cell proliferation and immediate onset of neoplasia. In contrast, in adult mice MYC overexpression induced cell growth and DNA replication without mitotic cell division, and mice succumbed to neoplasia only after a prolonged latency. In adult hepatocytes, MYC activation failed to induce cell division, which was at least in part mediated through the activation of p53. Surprisingly, apoptosis is not a barrier to MYC inducing tumorigenesis. The ability of oncogenes to induce tumorigenesis may be generally restrained by developmentally specific mechanisms. Adult somatic cells have evolved mechanisms to prevent individual oncogenes from initiating cellular growth, DNA replication, and mitotic cellular division alone, thereby preventing any single genetic event from inducing tumorigenesis

Transmembrane protein PERP is a component of tessellate junctions and of other junctional and non-junctional plasma membrane regions in diverse epithelial and epithelium-derived cells

Protein PERP (p53 apoptosis effector related to PMP-22) is a small (21.4 kDa) transmembrane polypeptide with an amino acid sequence indicative of a tetraspanin character. It is enriched in the plasma membrane and apparently contributes to cell-cell contacts. Hitherto, it has been reported to be exclusively a component of desmosomes of some stratified epithelia. However, by using a series of newly generated mono- and polyclonal antibodies, we show that protein PERP is not only present in all kinds of stratified epithelia but also occurs in simple, columnar, complex and transitional epithelia, in various types of squamous metaplasia and epithelium-derived tumors, in diverse epithelium-derived cell cultures and in myocardial tissue. Immunofluorescence and immunoelectron microscopy allow us to localize PERP predominantly in small intradesmosomal locations and in variously sized, junction-like peri- and interdesmosomal regions (“tessellate junctions”), mostly in mosaic or amalgamated combinations with other molecules believed, to date, to be exclusive components of tight and adherens junctions. In the heart, PERP is a major component of the composite junctions of the intercalated disks connecting cardiomyocytes. Finally, protein PERP is a cobblestone-like general component of special plasma membrane regions such as the bile canaliculi of liver and subapical-to-lateral zones of diverse columnar epithelia and upper urothelial cell layers. We discuss possible organizational and architectonic functions of protein PERP and its potential value as an immunohistochemical diagnostic marker

Adult Spinal Cord Radial Glia Display a Unique Progenitor Phenotype

Radial glia (RG) are primarily embryonic neuroglial progenitors that express Brain Lipid Binding Protein (Blbp a.k.a. Fabp7) and Glial Fibrillary Acidic Protein (Gfap). We used these transcripts to demarcate the distribution of spinal cord radial glia (SCRG) and screen for SCRG gene expression in the Allen Spinal Cord Atlas (ASCA). We reveal that neonatal and adult SCRG are anchored in a non-ventricular niche at the spinal cord (SC) pial boundary, and express a “signature” subset of 122 genes, many of which are shared with “classic” neural stem cells (NSCs) of the subventricular zone (SVZ) and SC central canal (CC). A core expressed gene set shared between SCRG and progenitors of the SVZ and CC is particularly enriched in genes associated with human disease. Visualizing SCRG in a Fabp7-EGFP reporter mouse reveals an extensive population of SCRG that extend processes around the SC boundary and inwardly (through) the SC white matter (WM), whose abundance increases in a gradient from cervical to lumbar SC. Confocal analysis of multiple NSC-enriched proteins reveals that postnatal SCRG are a discrete and heterogeneous potential progenitor population that become activated by multiple SC lesions, and that CC progenitors are also more heterogeneous than previously appreciated. Gene ontology analysis highlights potentially unique regulatory pathways that may be further manipulated in SCRG to enhance repair in the context of injury and SC disease

Axonal Control of the Adult Neural Stem Cell Niche

SUMMARYThe ventricular-subventricular zone (V-SVZ) is an extensive germinal niche containing neural stem cells (NSC) in the walls of the lateral ventricles of the adult brain. How the adult brain’s neural activity influences the behavior of adult NSCs remains largely unknown. We show that serotonergic (5HT) axons originating from a small group of neurons in the raphe form an extensive plexus on most of the ventricular walls. Electron microscopy revealed intimate contacts between 5HT axons and NSCs (B1) or ependymal cells (E1) and these cells were labeled by a transsynaptic viral tracer injected into the raphe. B1 cells express the 5HT receptors 2C and 5A. Electrophysiology showed that activation of these receptors in B1 cells induced small inward currents. Intraventricular infusion of 5HT2C agonist or antagonist increased or decreased V-SVZ proliferation, respectively. These results indicate that supraependymal 5HT axons directly interact with NSCs to regulate neurogenesis via 5HT2C

Plakophilin3 Loss Leads to an Increase in PRL3 Levels Promoting K8 Dephosphorylation, Which Is Required for Transformation and Metastasis

The desmosome anchors keratin filaments in epithelial cells leading to the formation of a tissue wide IF network. Loss of the desmosomal plaque protein plakophilin3 (PKP3) in HCT116 cells, leads to an increase in neoplastic progression and metastasis, which was accompanied by an increase in K8 levels. The increase in levels was due to an increase in the protein levels of the Phosphatase of Regenerating Liver 3 (PRL3), which results in a decrease in phosphorylation on K8. The increase in PRL3 and K8 protein levels could be reversed by introduction of an shRNA resistant PKP3 cDNA. Inhibition of K8 expression in the PKP3 knockdown clone S10, led to a decrease in cell migration and lamellipodia formation. Further, the K8 PKP3 double knockdown clones showed a decrease in colony formation in soft agar and decreased tumorigenesis and metastasis in nude mice. These results suggest that a stabilisation of K8 filaments leading to an increase in migration and transformation may be one mechanism by which PKP3 loss leads to tumor progression and metastasis