Prom Adam Smith to-Mayhard 'Kcynes : the heritage of political economy.

LB.6

The Ranger, a collection of periodical essays : inscribed to the Rev. Thomas Atwood, M.A. by the Hon. M. Hawke, and Sir R. Vincent, Bart. ...

"This gentleman [i.e. Martin Bladen Hawke] commenced his literary career at an early age; for while under the tuition of the Rev. Mr. Atwood, ... he published in association with his fellow pupil, the late Sir F. Fincent, a series of periodical essays, ..." ('A biographical dictionary of living authors', London: 1816, p. 149)Authors and publishers: The Hon. Martin Bladen Hawke, and Sir Francis Vincent, Bart. [Sir R. Vincent = Sir Francis Vincent].Dedication in vol. I signed by the authors.Imprints lack dates; year of publication from reference sources.Moral and ethical standards and social conduct, discussed in essays and anecdotes.With contents table and errata leaf in each volume.Gap in publication between July 5, 1794 (no. 28) and Jan. 3, 1795 (no. 29).Volumes lack chronological designations or dates.Collects weekly issues of The Ranger, with added prefatory material

Cardiac Functions of Voltage-Gated Ca2+ Channels: Role of the Pharmacoresistant Type (E-/R-Type) in Cardiac Modulation and Putative Implication in Sudden Unexpected Death in Epilepsy (SUDEP)

Voltage-gated Ca2+ channels (VGCCs) are ubiquitous in excitable cells. These channels play key roles in many physiological events like cardiac regulation/ pacemaker activity due to intracellular Ca2+ transients. In the myocardium, the Cayl subfamily (L-type: C41.2 and C41.3) is the main contributor to excitation contraction coupling and/or pacemaking, whereas the Ca(v)3 subfamily (T-type: Cay3.1 and Cay3.2) is important in rhythmically firing of the cardiac nodal cells. No established cardiac function has been attributed to the Ca(v)2 family (E-/R-type: Ca(v)2.3) despite accumulating evidence of cardiac dysregulation observed upon deletion of the Ca(v)2.3 gene, the only member of this family so far detected in cardiomyocytes. In this review, we summarize the pathophysiological changes observed after ablation of the E-/R-type VGCC and propose a cardiac mechanism of action for this channel. Also, considering the role played by this channel in epilepsy and its reported sensitivity to antiepileptic drugs, a putative involvement of this channel in the cardiac mechanism of sudden unexpected death in epilepsy is also discussed