A death and a marriage: an examination of the literature occasioned by the death of Henry Prince of Wales and the marriage of his sister Princess Elizabeth, 1612-13

This dissertation examines the occasional literature - elegies, sermons, marriage poems, Basques, and pamphlets - composed on the death of Henry Prince of Wales in November 1612, and the marriage of his sister, Princess Elizabeth, to Frederick V Elector Palatine, in the following February. An attempt has beon made to note the themes, conventions and images commonly used in the literature, and the way in which individual writers and poets handle them has been discussed. In addition the relationship between the personalities of the Prince and Princess, in so far as they can be ascertained, and the view of them presented to the reader by the literature has been explored. The far reaching political and religious implications of the events, dwelt on at considerable length by a number of writers and poets, have also been discussed in so far as they are reflected in the prose and verse written for the occasions. The relevant social background of the contributors to the bodies of literature, together with that of their patrons and dedicatees has also been explored in an attempt to discover the relationship of writers and patrons to the events, and so offer a partial explanation for the remarkable outpouring of commemorative volumes. Finally the imaginative literature of the years 1612-15 has been examined In order to trace the influence of the events in a wider field

cAMP-dependent Protein Kinase Activation Lowers Hepatocyte cAMP

Rat hepatocyte protein kinase was activated by incubating the cells with various cAMP analogs. Boiled extracts were then prepared and Sephadex G-25 chromatography was carried out. The G-25 procedure separated the analogs from cAMP since the resin had the unexpected property of binding cyclic nucleotides with differing affinities. Separation was necessary because the analogs would otherwise interfere with the sensitive protein kinase activation method developed for assay of cAMP. The cAMP analogs, but not 5\u27-AMP, lowered basal cAMP by 50-70%. The effect was rapid, analog concentration-dependent, and occurred parallel with phosphorylase activation, suggesting that the cAMP analogs act through cAMP-dependent protein kinase activation. A cAMP analog completely blocked the cAMP elevation produced by relatively low concentrations of glucagon, but did not block the phosphorylase response, indicating that the cAMP analog substitutes for cAMP as the intracellular activator of protein kinase. One implication of the results is that elevation of cAMP and protein kinase activity by hormones has a negative feedback effect on the cellular cAMP level

Atom Interferometric Imaging of Differential Potentials Using an Atom Laser

Interferometry is a prime technique for modern precision measurements. Atoms, unlike light, have significant interactions with electric, magnetic, and gravitational fields, making their use in interferometric applications particularly versatile. Here, we demonstrate atom interferometry to image optical and magnetic potential landscapes over an area exceeding $240 \mu m \times 600 \mu m$. The differential potentials employed in our experiments generate phase imprints in an atom laser that are made visible through a Ramsey pulse sequence. We further demonstrate how advanced pulse sequences can enhance desired imaging features, e.g. to image steep potential gradients. A theoretical discussion is presented that provides a semiclassical analysis and matching numerics.Comment: Updated to match published version. 13 pages, 9 figure

Algae: Causes and Complications

This panel will explore the causes of algal blooms, the threats they present to Virginia’s waters, and steps being taken to address them

Discriminative Insulin Antagonism of Stimulatory Effects of Various cAMP Analogs on Adipocyte Lipolysis and Hepatocyte Glycogenolysis

Although insulin effectively blocked hormone-stimulated glycerol output in adipocytes or phosphorylase activation in hepatocytes, the inhibitory effect of insulin on cAMP analog-stimulated cells depended on the cAMP analog used. Of the 20 analogs tested in adipocytes and 13 tested in hepatocytes, the effects of about half of them were effectively blocked by insulin, whereas the effects of many of them were not inhibited at all. In order to approach the explanation for this discriminative insulin action, the inhibitory effects of insulin on the responses to the analogs in the intact cells were correlated with the in vitro cAMP analog specificity for the hepatocyte cAMP-dependent protein kinase isozymes and the low K(m), hormone-sensitive phosphodiesterases from both cell types. No correlation was found between insulin resistance of analog-stimulated hepatocyte phosphorylase and the concentration of analog required in vitro for half-maximal activation of either type I or type II cAMP-dependent protein kinase from hepatocytes. However, a good correlation was found between insulin resistance of cAMP analog-stimulated responses and the analog I50 values for the phosphodiesterase from both cell types. Using a new method capable of measuring hydrolysis at low analog concentrations, several of those analogs which had relatively low, but not high, phosphodiesterase I50 values were shown to be directly hydrolyzed by the low K(m) adipocyte phosphodiesterase. The insulin inhibition of cell responses when stimulated by hydrolyzable analogs, but not by poorly hydrolyzable analogs, is best explained by insulin stimulation of the low K(m) phosphodiesterases from both cell types

Lifelong behavioral and neuropathological consequences of repetitive mild traumatic brain injury

Objective: Exposure to repetitive concussion, or mild traumatic brain injury (mTBI), has been linked with increased risk of long-term neurodegenerative changes, specifically chronic traumatic encephalopathy (CTE). To date, preclinical studies largely have focused on the immediate aftermath of mTBI, with no literature on the lifelong consequences of mTBI in these models. This study provides the first account of lifelong neurobehavioral and histological consequences of repetitive mTBI providing unique insight into the constellation of evolving and ongoing pathologies with late survival. Methods: Male C57BL/6J mice (aged 2–3 months) were exposed to either single or repetitive mild TBI or sham procedure. Thereafter, animals were monitored and assessed at 24 months post last injury for measures of motor coordination, learning deficits, cognitive function, and anxiety-like behavior prior to euthanasia and preparation of the brains for detailed neuropathological and protein biochemical studies. Results: At 24 months survival animals exposed to r-mTBI showed clear evidence of learning and working memory impairment with a lack of spatial memory and vestibule-motor vestibulomotor deficits compared to sham animals. Associated with these late behavioral deficits there was evidence of ongoing axonal degeneration and neuroinflammation in subcortical white matter tracts. Notably, these changes were also observed after a single mTBI, albeit to a lesser degree than repetitive mTBI. Interpretation: In this context, our current data demonstrate, for the first time, that rather than an acute, time limited event, mild TBI can precipitate a lifelong degenerative process. These data therefore suggest that successful treatment strategies should consider both the acute and chronic nature of mTBI

Short-Term Feedback Regulation of cAMP by Accelerated Degradation in Rat Tissues

A recent study showed that cAMP analogs lowered cAMP levels in rat hepatocytes. The present work demonstrates that cAMP analogs also lowered cAMP in a rapid, concentration-dependent manner in heart and fat cells. In order to determine if the cAMP-dependent protein kinase mediated this effect, techniques were developed to assay the protein kinase activity ratio in hepatocytes treated with cAMP analogs. The activation of protein kinase and phosphorylase in hepatocytes by 8-pClΦS-cAMP (where 8-pClΦS- indicates 8-parachlorothiophenyl-) was concentration-dependent and occurred in parallel to proportionate decreases in cAMP. More than 20% of the cAMP binding sites on the protein kinase were unoccupied at concentrations of 8-pClΦS-cAMP that produced maximal cAMP lowering. Thus, the possibility that 8-pClΦS-cAMP lowered cAMP by displacing it from protein kinase binding sites, making it available for hydrolysis, seemed unlikely. In adipocytes, the lowering of cAMP by 8-pClΦS-cAMP occurred in parallel with increases in lipolysis and activation of low K(m) phosphodiesterase, suggesting that the phosphodiesterase was responsible for the cAMP lowering. Further evidence for this assertion was the finding that in hepatocytes preloaded with low concentrations of 8-pClΦS-cAMP, glucagon lowered 8-pClΦS-cAMP by about 50%, an amount similar to the cAMP lowering observed with 8-pClΦS-cAMP treatment. The results were consistent with a cAMP-dependent protein kinase-catalyzed activation of a phosphodiesterase and suggested that 8-pClΦS-cAMP-mediated hydrolysis of cAMP mimicked a physiologically significant response. The observation of this phenomenon in several tissues further suggested that it may a general mechanism for dampening and terminating the hormonal signal through accelerated degradation of cAMP