Catalogue of shield reptiles in the collection of the British museum. Pt. I. Testudinata (tortoises)

Accompanied by "Supplement to the Catalogue of shield reptiles in the collection of the British museum. Pt. I. Testudinata (tortoises). With figures of the skulls of 36 genera. By John Edward Gray." (ix, [1], 120 p. illus. 31 x 25 cm.) Published: London, Printed by order of the Trustees, 1870.

Addresses of John Hay.

I. Franklin in France.--II. Omar Khayyám.--III. Sir Walter Scott.--IV. Speeches before the American society in London.--V. A partnership in beneficence.--VI. Speech at the annual dinner of the Royal society.--VII. Speech at the annual dinner of the Literary fund.--VIII. Speech at the opening, by Miss Helen Hay, of the Robert Browning garden.--IX. International copyright.--X. American diplomacy.--XI. A festival of pece.--XII. William McKinley.--XIII. At the universities.--XIV. Commercial club dinner.--XV. New Orleans.--XVI. The Grand army of the republic.--XVII. President Roosevelt.--XVIII. Edmund Clarence Stedman.--XIX. Lincoln's faith.--XX. The press and modern progress.--XXI. Fifty years of the Republican party.--XXII. America's love of peace.--XXIII. Life in the White House in the time of Lincoln.--XXIV. Clarence King.

The works of William Makepeace Thackeray /

Each volume has special t.-p.

Porcupine's works : containing various writings and selections, exhibiting a faithful picture of the United States of America; of their governments, laws, politics and resources; of the characters of their presidents, governors, legislators, magistrates, and military men; and of the customs, manners, morals, religion, virtues and vices of the people : comprising also a complete series of historical documents and remarks, from the end of the war, in 1783, to the election of the President, in March, 1801 /

continued: ... XII. Historical documents and remarks (from December, 1799 to March, 1801) ; Trial of Cooper ; Emigration Society ; Washington's death ; Proceedings in Congress during the session which began December, 1799 ; Board of Commissioners ; Defence of the Quakers of Pennsylvania ; Farewell advertisement ; Prison eclogue ; Republican morality ; Jefferson's election ; Adam's public conduct ; Jefferson's character ; Convention concluded between America and France, in 1800 ; Proceedings in Congress during the session which ended in March, 1801 ; Index.

The extant poetical works of William Lauder, playwright, poet, and minister of the word of God ...

Each part issued separately, with special t.-p. and separate pagination.

Final concords of the County of Lancashire, from the original chirographs, or feet of fines preserved in the Public Record Office, London.

"Additions and corrections": [1] p. inserted in pt. 1 between p. [vi] and [vii]

Account of the expenses of John of Brabant and Thomas and Henry of Lancaster, A.D. 1292-3.

Forms part of the Society's Publication no. LV

Second book of airs : 1600 /

"General preface" and "Preface to Dowland's Second book of songs or airs": at beginning of each vol.

Talvi's History of the colonization of America.

Talvj, pseud. of the author.

Duke Christian of Luneburg;

Mode of access: Internet.

Letters of the Duke and Duchess of Buckingham,

Only 51 copies printed.

Collections relative to claims at the coronations of several of the kings of England, beginning with King Richard II.

"Exhibiting ... from authentic sources, claims made at several of the coronations of our kings, from Richard II ... to that of George II." --Advertisement.

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.