19,145 research outputs found
Letter from Thomas J. Croaff to Carl Hayden
Letter from attorney Thomas J. Croff to Carl Hayden informing him of the Atchison, Topeka, and Santa Fe railroad company's ownership of land inside the proposed national park boundaries
Western medieval legal manuscripts in the collections of the University of Pennsylvania
Western legal manuscripts of the Middle Ages in North American collections are among the least known to scholars. The University of Pennsylvania has a rich collection of these texts, several of which were in the collection of the historian Henry Charles Lea. Included are works of civil law and canon law, as well as collections of papal letters and guides to pastoral care. The descriptions of most of these manuscripts in the catalog of Norman P. Zacour and Rudolf Hirsch are perfunctory, sometimes erring or omitting valuable information. Other manuscripts were added in recent years in the Lawrence J. Schoenberg Collection. Much of this material is being added to the Franklin online catalog of the University’s libraries, but researchers frequently do not search these digital resources. This article provides more complete guidance to the University’s medieval legal manuscripts than any of the existing catalogs offers, whether in print or online. It also provides updated bibliographic information in print or online. Every manuscript has been examined by the author in situ. Among the important works represented in the collection is the Panormia (a work of canon law often attributed to Ivo of Chartres). Authors present include the curialist Thomas of Capua, canonists Petrus de Braco, William of Pagula, Bernardus Raimundi, Adam of Aldersbach, Raymond of Peñafort, and civil lawyers Baldus de Ubaldis, and Bartolus de Saxoferrato. Three of these manuscripts were owned in the past by Sir Thomas Phillipps
Author Thomas Dixon, Jr.
Author Thomas Dixon, Jr.To order a reproduction, inquire about permissions, or for information about prices see:
http://www.lib.washington.edu/specialcollections/services/reproduction/reproduction
Please cite the Order NumberScanned at 600ppi with an Epson 20000 flatbed scanner. Image then rotated, cropped, level-adjusted, and sharpened using Photoshop CS3. Converted to a JPEG2000 image upon ingest into CONTENTdm
Contribution of JAM-1 to epithelial differentiation and tight-junction biogenesis in the mouse preimplantation embryo
We have investigated the contribution of the tight junction (TJ) transmembrane protein junction-adhesion-molecule 1 (JAM-1) to trophectoderm epithelial differentiation in the mouse embryo. JAM-1-encoding mRNA is expressed early from the embryonic genome and is detectable as protein from the eight-cell stage. Immunofluorescence confocal analysis of staged embryos and synchronized cell clusters revealed JAM-1 recruitment to cell contact sites occurred predominantly during the first hour after division to the eight-cell stage, earlier than any other TJ protein analysed to date in this model and before E-cadherin adhesion and cell polarization. During embryo compaction later in the fourth cell cycle, JAM-1 localized transiently yet precisely to the apical microvillous pole, where protein kinase C (PKC) and PKC are also found, indicating a role in cell surface reorganization and polarization. Subsequently, in morulae and blastocysts, JAM-1 is distributed ubiquitously at cell contact sites within the embryo but is concentrated within the trophectoderm apicolateral junctional complex, a pattern resembling that of E-cadherin and nectin-2. However, treatment of embryos with anti-JAM-1-neutralizing antibodies indicated that JAM-1 did not contribute to global embryo compaction and adhesion but rather regulated the timing of blastocoel cavity formation dependent upon establishment of the trophectoderm TJ paracellular seal
Comprehensive behavioral testing in the R6/2 mouse model of Huntington's disease shows no benefit from CoQ10 or minocycline
Previous studies of the effects of coenzyme Q10 and minocycline on mouse models of Huntington’s disease have produced conflicting results regarding their efficacy in behavioral tests. Using our recently published best practices for husbandry and testing for mouse models of Huntington’s disease, we report that neither coenzyme Q10 nor minocycline had significant beneficial effects on measures of motor function, general health (open field, rotarod, grip strength, rearing-climbing, body weight and survival) in the R6/2 mouse model. The higher doses of minocycline, on the contrary, reduced survival. We were thus unable to confirm the previously reported benefits for these two drugs, and we discuss potential reasons for these discrepancies, such as the effects of husbandry and nutrition
Early Risk, Attention, and Brain Activation in Adolescents Born Preterm
The relations among early cumulative medical risk, cumulative environmental risk, attentional control, and brain activation were assessed in 15 – 16-year-old adolescents who were born preterm. Functional magnetic resonance imaging found frontal, temporal, and parietal cortex activation during an attention task with greater activation of the left superior-temporal and left supramarginal gyri associated with better performance. Individual differences in early cumulative risk are related to patterns of brain activation such that medical risk is related to left parietal cortex activation and environmental risk is related to temporal lobe activation. The findings suggest that early risk is related to less mature patterns of brain activation, including reduced efficiency of processing and responding to stimuli.This is the accepted version of the following article: Carmody, D. P., Bendersky, M., Dunn, S. M., DeMarco, J. K., Hegyi, T., Hiatt, M. and Lewis, M. (2006), Early Risk, Attention, and Brain Activation in Adolescents Born Preterm. Child Development, 77: 384–394, which has been published in final form at http://onlinelibrary.wiley.com/doi/10.1111/j.1467-8624.2006.00877.x/abstract.Peer reviewe
Letter from an unknown author to Thomas J. Goree concerning information on specific regimetns and battles in the Civil War.
Letter from an unknown author to Thomas J. Goree asking for information on specific battles and regiments in the Civil War. The author thanks Goree for his reply and agreement to help provide information pertaining to a project the author has taken on. The author expresses that he feels as though he has taken on a much bigger task than he anticipated, and needs as much help as possible in acquiring information
Towards an understanding of protein kinase B (PKB/Akt) function in mouse development
Protein kinase B (PKB/Akt) belongs to a subfamily of serine/threonine protein kniases called AGC protein kinases. Homologues of PKB can be found in worms, flies and mammals. Three isoforms of PKB, termed PKBα/Akt1, PKBβ/Akt2 and PKBγ/Akt3 that are encoded by three distinct genes, have been identified in mammals like mice and humans. PKB can be activated by numerous growth factors, hormones, cytokines and other stimuli through a phosphatidylinositol 3-kinase (PI3K)-dependent manner. The signaling pathway of PI3K/PKB/Akt has been established and the significance of this pathway for numerous cellular and physiological processes has been recognized and widely accepted. The understanding of developmental principles in mouse is a big challenge. How PKB contributes to mouse development and why three isoforms exist in mice have been wondering researchers in this field since the identification of these proteins in this animal. Early mouse work using northern blotting and in situ hybridization showed expression of PKB/Akt in mouse embryos with isoform- and tissue-specific properties. Thus, PKB/Akt may play important roles in mouse development. In addition, the distinct tissue distribution patterns of the three isoforms suggest that these proteins have different functions. To address these questions, we generated mouse mutant for each isoform by homologous recombination. Characterization and analyses of these mice have provided new insights into the functions of PKB/Akt in mouse development. We found that PKBα/Akt1 was the predominant isoform in placenta. PKBα/Akt1 mutant mice were born small with increased neonatal mortality. The mutant placenta displayed reduced size and impaired development and glycogen-containing spongiotrophoblast cells are
rare. More significant is a decrease in vascularization of the mutant placenta. As the
size and structure of the placenta determines the growth of the fetus, we conclude that
PKBα/Akt1 modulates placental development and, thus, fetal growth.
In contrast to PKBα/Akt1 mutant mice, PKBγ/Akt3 mutant mice did not show
increased postnatal mortality and and grew normally. However, these mice displayed a
reduced brain size by 25% after birth. This indicates that PKBγ/Akt3 is an important
modulator of postnatal brain growth.
We crossed PKBα/Akt1 mutant mice with PKBγ/Akt3 mutant mice to produce
compound knockout mice and found that the two proteins have different roles in the
maintenance of animal survival. While Pkbα+/−Pkbγ −/− (Akt1+/-Akt3 -/-) mice survived
normally, almost all Pkbα -/-Pkbγ +/-(Akt1-/- Akt3+/-) mice died at an early age with
multiple pathologies. PKBα/γ (Akt1/3) double knockout mice were embryonic lethal at
around E12. The development of these mice was severely impaired, including the
branchial arch arteries, the brain and the placenta. We conclude that PKBα/Akt1 is
more important than PKBγ/Akt3 for animal survival but both are required for mouse
development
Corticotropin-releasing factor receptors couple to multiple g-proteins to activate diverse intracellular signaling pathways in mouse hippocampus: role in neuronal excitability and associative learning
Corticotropin-releasing factor (CRF) exerts a key neuroregulatory control on stress responses in various regions of the mammalian brain, including the hippocampus. Using hippocampal slices, extracts, and whole animals, we investigated the effects of human/rat CRF (h/rCRF) on hippocampal neuronal excitability and hippocampus-dependent learning in two mouse inbred strains, BALB/c and C57BL/6N. Intracellular recordings from slices revealed that application of h/rCRF increased the neuronal activity in both mouse inbred strains. Inhibition of protein kinase C (PKC) by bisindolylmaleimide I (BIS-I) prevented the h/rCRF effect only in hippocampal slices from BALB/c mice but not in slices from C57BL/6N mice. Inhibition of cAMP-dependent protein kinase (PKA) by H-89 abolished the h/rCRF effect in slices from C57BL/6N mice, with no effect in slices from BALB/c mice. Accordingly, h/rCRF elevated PKA activity in hippocampal slices from C57BL/6N mice but increased only PKC activity in the hippocampus of BALB/c mice. These differences in h/rCRF signal transduction were also observed in hippocampal membrane suspensions from both mouse strains. In BALB/c mice, hippocampal CRF receptors coupled to Gq/11 during stimulation by h/rCRF, whereas they coupled to Gs, Gq/11, and Gi in C57BL/6N mice. As expected on the basis of the slice experiments, h/rCRF improved context-dependent fear conditioning of BALB/c mice in behavioral experiments, and BIS-I prevented this effect. However, although h/rCRF increased neuronal spiking in slices from C57BL/6N mice, it did not enhance conditioned fear. These results indicate that the CRF system activates different intracellular signaling pathways in mouse hippocampus and may have distinct effects on associative learning depending on the mouse strain investigated
Atheist: or, The second part of the Souldiers fortune
Otway, Thomas (1652-1685) London: Printed for R. Bentley and J. Tonson, 1684 University of Utah copy bound with the author\u27s The Souldiers Fortune. London, 168
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