Friedrich II. von Preussen und Peter III.

Vita.

History of Friedrich the Second, called Frederick the Great,

Mode of access: Internet.

Rheinsberg: memeorials of Frederick the Great and Prince of Prussia.

Mode of access: Internet.

Studies in word-association; experiments in the diagnosis of psychopathological conditions carried out at the Psychiatric clinic of the University of Zurich, under the direction of C.G. Jung ...

"This book is a translation of a series of papers on the results of the association method applied to normal and abnormal persons, which appeared in the Journal für psychologie und neurologie (vols. III-XVI) and were afterwards collectecd into two volumes."--Translator's pref.

Li︠u︡dovik II, korolʹ bavarskiĭ : k istorīi zhizni i tvorchestva Rikharda Vagnera /

Romanized record.

Diary and correspondence of John Evelyn, F.R.S., to which is subjoined the private correspondence between King Charles I and Sir Edward Nicholas, and between Sir Edward Hyde, afterwards Earl of Clarendon, and Sir Richard Browne.

Half-title of v. 4: Bohn's historical library.

Saint Edmund king and martyr; a history of his life and times with an account of the translation of his incorrupt body, etc. From original mss.,

Mode of access: Internet.

Literary remains of King Edward the Sixth. Edited from his autograph manuscripts, with historical notes and a biographical memoir,

This ed. was originally printed for the Roxburghe Club in 1857.

Letters and poems of Queen Elisabeth (Carmen Sylva)

"Poems ('Vers libre') by Carmen Sylva": vol. II, p. 175-222.

Frederick the Great, the memoirs of his reader, Henri de Catt (1758-1760)

Translation of: Unterhaltungen mit Friedrich dem Grossen.

Report to the Right Hon. the Lord Chief Baron, and the Hon. the Barons of His Majesty's Court of Exchequer in Scotland, by the King's Remembrancer, relative to the tomb of King Robert the Bruce, and the Cathedral Church of Dunfermline.

Mode of access: Internet.

Particle size of Saharan dust in the Atlantic Ocean, from October 2012 to November 2013

Mineral dust has a large impact on regional and global climate, depending on its particle size. Especially in the Atlantic Ocean downwind of the Sahara, the largest dust source on earth, the effects can be substantial but are poorly understood. This study focuses on seasonal and spatial variations in particle size of Saharan dust deposition across the Atlantic Ocean, using an array of submarine sediment traps moored along a transect at 12° N. We show that the particle size decreases downwind with increased distance from the Saharan source, due to higher gravitational settling velocities of coarse particles in the atmosphere. Modal grain sizes vary between 4 and 33 µm throughout the different seasons and at five locations along the transect. This is much coarser than previously suggested and incorporated into climate models. In addition, seasonal changes are prominent, with coarser dust in summer, and finer dust in winter and spring. Such seasonal changes are caused by transport at higher altitudes and at greater wind velocities during summer than in winter. Also the latitudinal migration of the dust cloud, associated with the Intertropical Convergence Zone, causes seasonal differences in deposition as the summer dust cloud is located more to the north, and more directly above the sampled transect. Furthermore, increased precipitation and more frequent dust storms in summer coincide with coarser dust deposition. Our findings contribute to understanding Saharan dust transport and deposition relevant for the interpretation of sedimentary records for climate reconstructions, as well as for global and regional models for improved prediction of future climate.

Degradation of azo-dye Orange II by a photoassisted Fenton reaction using a novel composite of iron oxide and silicate nanoparticles as a catalyst

A novel nanocomposite of iron oxide and silicate, prepared through a reaction between a solution of iron salt and a dispersion of Laponite clay, was used as a catalyst for the photoassisted Fenton degradation of azo-dye Orange II. This catalyst is much cheaper than the Nafion-based catalysts, and our results illustrate that it can significantly accelerate the degradation of Orange II under the irradiation of UV light (lambda = 254 nm). An advantage of the catalyst is its long-term stability that was confirmed through using the catalyst for multiple runs in the degradation of Orange II. The effects of the H2O2 molar concentration, solution pH, wavelength and power of the LTV light, catalyst loading, and initial Orange II concentration on the degradation of Orange 11 were studied in detail. In addition, it was also found that discoloration of Orange 11 undergoes a faster kinetics than mineralization of Orange II and 75% total organic carbons of 0.1 mM Orange II can be eliminated after 90 min in the presence of 1.0 g of Fe-nanocomposite/L, 4.8 mM H2O2, and 1 x 8W UVC.

Investigation of signaling pathways that mediate the inotropic effect of urotensin-II in human heart

Objective: This study investigated signaling pathways that may contribute to the potent positive inotropic effect of human urotensin-II (hU-II) in human isolated right atrial trabeculae obtained from patients with coronary artery disease. Methods: Trabeculae were set up in tissue baths and stimulated to contract at 1 Hz. Tissues were incubated with 20 nM hU-II with or without phorbol 12-myristate 13-acetate (PMA, 10 muM) to desensitize PKC, the PKC inhibitor chelerythrine (10 muM), 10 muM 4alpha-phorbol that does not desensitize PKC, the myosin light chain kinase inhibitor wortmannin (50 nM, 10 muM), or the Rho kinase inhibitor Y-27632 (0.1 - 10 muM). Activated RhoA was determined by affinity immunoprecipitation, and phosphorylation of signaling proteins was determined by SDS-PAGE. Results: hU-II caused a potent positive inotropic response in atrial trabeculae, and this was concomitant with increased phosphorylation of regulatory myosin light chain (MLC-2, 1.8 +/- 0.4-fold, P < 0.05, n = 6) and PKCalpha/betaII (1.4 +/- 0.2-fold compared to non-stimulated controls, P < 0.05, n = 7). Pretreatment of tissues with PMA caused a marked reduction in the inotropic effect of hU-II, but did not affect hU-II-mediated phosphorylation of MLC-2. The inotropic response was inhibited by chelerythrine, but not 4alpha-phorbol or wortmannin. Although Y-27632 also reduced the positive inotropic response to hU-II, this was associated with a marked reduction in basal force of contraction. RhoA. GTP was immunoprecipitated in tissues pretreated with or without hU-II, with findings showing no detectable activation of RhoA in the agonist stimulated tissues. Conclusions: The findings indicated that hU-II increased force of contraction in human heart via a PKC-dependent mechanism and increased phosphorylation of MLC-2, although this was independent of PKC. The positive inotropic effect was independent of myosin light chain kinase and RhoA-Rho kinase signaling pathways. (C) 2004 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.

Mechanism of attenuation of angiotensin-II-induced protein degradation by insulin-like growth factor-I (IGF-I)

Insulin-like growth factor-I (IGF-I) has been shown to attenuate protein degradation in murine myotubes induced by angiotensin II through downregulation of the ubiquitin-proteasome pathway, although the mechanism is not known. Angiotensin II is known to upregulate this pathway through a cellular signalling mechanism involving release of arachidonic acid, activation of protein kinase Cα (PKCα), degradation of inhibitor-κB (I-κB) and nuclear migration of nuclear factor-κB (NF-κB), and all of these events were attenuated by IGF-I (13.2 nM). Induction of the ubiquitin-proteasome pathway has been linked to activation of the RNA-activated protein kinase (PKR), since an inhibitor of PKR attenuated proteasome expression and activity in response to angiotensin II and prevented the decrease in the myofibrillar protein myosin. Angiotensin II induced phosphorylation of PKR and of the eukaryotic initiation factor-2 (eIF2) on the α-subunit, and this was attenuated by IGF-I, by induction of the expression of protein phosphatase 1, which dephosphorylates PKR. Release of arachidonic acid and activation of PKCα by angiotensin II were attenuated by an inhibitor of PKR and IGF-I, and the effect was reversed by Salubrinal (15 μM), an inhibitor of eIF2α dephosphorylation, as was activation of PKCα. In addition myotubes transfected with a dominant-negative PKR (PKRΔ6) showed no release of arachidonate in response to Ang II, and no activation of PKCα. These results suggest that phosphorylation of PKR by angiotensin II was responsible for the activation of the PLA2/PKC pathway leading to activation of NF-κB and that IGF-I attenuates protein degradation due to an inhibitory effect on activation of PKR. © 2007 Elsevier Inc. All rights reserved.