The Molecular Pathology of Prion Diseases

Prion diseases, or transmissible spongiform encephalopathies (TSEs), are a group of invariably fatal neurodegenerative disorders. Uniquely, they may present as sporadic, inherited, or infectious forms, all of which involve conversion of the normal cellular prion protein (PrPC) into a pathogenic likeness of itself (PrPSc). Formation of neurotoxic PrPSc and/or loss of the normal function of native PrPC result in activation of cellular pathways ultimately leading to neuronal death. Prion diseases can affect both humans and animals, with scrapie of sheep, bovine spongiform encephalopathy (BSE), and Creutzfeldt-Jakob disease being the most notable. This review is intended to provide an overview of the salient scientific discoveries in prion research, mainly from a molecular perspective. Further, some of the major outstanding questions in prion science are highlighted. Prion research is having a profound impact on modern medicine, and strategies for prevention and treatment of these disorders may also find application in the more common neurodegenerative diseases.peer-reviewe

Emergence and Adult Biology of \u3ci\u3eAgrilus Difficilis\u3c/i\u3e (Coleoptera: Buprestidae), a Pest of Honeylocust, \u3ci\u3eGleditsia Triacanthos\u3c/i\u3e

Emergence and adult biology of Agrilus difficilis were examined in relation to its host Gleditsia triacanthos. began as early as 5 June in 1982 and completed as late as 22 July in 1983. Females lived significantly longer, 48 days, than males, 29 days. Average fecundity was one egg per day during a 36-day oviposition period

Saving a Tree Genus: Researchers Are Working Toward an Ash Hybrid Resistant to Emerald Ash Borer

Author Institution (Herms): Department of Entomology, The Ohio State University; Author Institution (Bonello): Department of Plant Pathology, The Ohio State Universit

The CCD sensor: A semiconductor circuit for capturing images. On the Nobel Prize in Physics awarded to Charles Kuen Kao, Willard S. Boyle, and George E. Smith (II)

The Nobel Prize in Physics 2009 was jointly awarded to two scientists (in addition to Charles Kuen Kao): Willard S. Boyle and George E. Smith, both of Bell Laboratories in Murray Hill, New Jersey, for having invented, in 1969, an imaging semiconductor circuit, the CCD (charge-coupled device), an electronic device which allowed an important development of digital cameras, both photography and video. A year later, Bell Labs already had the first CCD-based camcorder. In commercial cameras it is being replaced by CMOS sensors, but in some capture systems it is still the most important component, especially because of its low levels of noise. This article examines the functioning and evolution of the device.El Premi Nobel de Física 2009 va atorgar el guardó compartit a dos científics (a més de Charles Kuen Kao): Willard S. Boyle i George E. Smith, ambdós dels laboratoris Bell de Murray Hill, a Nova Jersey, per haver inventat, el 1969, un dispositiu electrònic, el sensor CCD (charge-coupled device o ‘dispositiu de càrrega acoblada'), que ha permès un desenvolupament important de les càmeres digitals, tant de fotografia com de vídeo. Només un any més tard, els laboratoris Bell ja tenien en funcionament la primera videocàmera basada en CCD. En càmeres comercials està essent substituït per sensors CMOS, però en certs sistemes de captura encara és el més important, especialment pel baix nivell de soroll. En aquest article s'analitza el funcionament del dispositiu i l'evolució que té

Monoacylated Cellular Prion Proteins Reduce Amyloid-beta-Induced Activation of Cytoplasmic Phospholipase A2 and Synapse Damage

Alzheimer’s disease (AD) is a progressive neurodegenerative disease characterized by the accumulation of amyloid-β (Aβ) and the loss of synapses. Aggregation of the cellular prion protein (PrPC) by Aβ oligomers induced synapse damage in cultured neurons. PrPC is attached to membranes via a glycosylphosphatidylinositol (GPI) anchor, the composition of which affects protein targeting and cell signaling. Monoacylated PrPC incorporated into neurons bound “natural Aβ”, sequestering Aβ outside lipid rafts and preventing its accumulation at synapses. The presence of monoacylated PrPC reduced the Aβ-induced activation of cytoplasmic phospholipase A2 (cPLA2) and Aβ-induced synapse damage. This protective effect was stimulus specific, as treated neurons remained sensitive to α-synuclein, a protein associated with synapse damage in Parkinson’s disease. In synaptosomes, the aggregation of PrPC by Aβ oligomers triggered the formation of a signaling complex containing the cPLA2.a process, disrupted by monoacylated PrPC. We propose that monoacylated PrPC acts as a molecular sponge, binding Aβ oligomers at the neuronal perikarya without activating cPLA2 or triggering synapse damage

Susceptibility of the Endangered Karner Blue Butterfly (Lepidoptera: Lycaenidae) to \u3ci\u3eBacillus Thuringiensis\u3c/i\u3e Var. \u3ci\u3eKurstaki\u3c/i\u3e Used for Gypsy Moth Suppression in Michigan

We investigated the phenological and physiological susceptibility of the endangered Karner blue butterfly (Lycaeides melissa samuelis) to Bacillus thuringiensis var. kurstaki (Bt), a product widely used for gypsy moth (Lymantria dispar) suppression in Michigan and other infested states. We monitored phenology of the bivoltine Karner blue in two regions of Michigan from 1993 to 1995 to determine if larval stages overlapped temporally with the period of Bt application for gypsy moth suppression. Karner blue larvae of the spring generation were found during the period that Bt was applied in nearby areas in 1993 only. However, spring-generation adults or newly laid eggs were observed up to 11 days before applications in 1994 and 1995. Since Karner blue eggs develop within one week, summer-generation larvae were most likely present during or shortly after 1994 and 1995 Bt application periods. These larvae would have been at risk, assuming Bt persistence of 4 to 6 days. Physiological susceptibility of Karner blue larvae to Bt was determined in a laboratory bioassay. Larvae were reared on wild lupine (Lupinus perennis) foliage that was untreated, or sprayed with Bt formulations at rates of 30-37 or 90 BIU/ha. A similar bioassay with second instar gypsy moth larvae on similarly treated white oak (Quercus alba) foliage was conducted concurrently. Karner blue survival was 100%, 27% and 14% on control, low and high Bt treatments, respectively. Early and late Karner blue instars were equally susceptible to Bt. Survival of gypsy moth was 80%, 33% and 5% on control, low and high Bt treatments, respectively, and did not differ significantly from Karner blue survival. We conclude that Karner blue is both phenologically and physiologically susceptible to Bt used for gypsy moth suppression, although the larval generation at risk and extent of phenological overlap may vary from year to year