4 resultados para Provoked vestibulodynia

em University of Queensland eSpace - Australia


Relevância:

10.00% 10.00%

Publicador:

Resumo:

The article makes the case for redescribing Jean Barbeyrac [1674-1744], the great French translator and influential glossator of seventeenth-century Latin natural-law texts, as something quite other than a neutral mediator of Samuel Pufendorf. To consider the specific religious and political charge of his strategies as translator is to recognize the independence of Barbeyrac's Huguenot stance on natura; jurisprudence. This stance is provoked by the profound challenge that Pufendorf's radical post-Wespthalian secularizing of civil authority posed for a Huguenot: how to grant that the state had legitimate authority to regulate all external conduct, but at the same time preserve an inviolable moral space for the exercise of individual conscience. The argument--pointing to Barbeyrac's construction of a 'Lockeanized' Pufendorf--rests both on his famous presentation of Leibniz's critique of Pufendorf's De officio hominis et civis and on more neglected elements of Barbeyrac's corpus.

Relevância:

10.00% 10.00%

Publicador:

Resumo:

This paper investigates the hypotheses that the recently established Mexican stock index futures market effectively serves the price discovery function, and that the introduction of futures trading has provoked volatility in the underlying spot market. We test both hypotheses simultaneously with daily data from Mexico in the context of a modified EGARCH model that also incorporates possible cointegration between the futures and spot markets. The evidence supports both hypotheses, suggesting that the futures market in Mexico is a useful price discovery vehicle, although futures trading has also been a source of instability for the spot market. Several managerial implications are derived and discussed. (C) 2004 Elsevier B.V. All rights reserved.

Relevância:

10.00% 10.00%

Publicador:

Resumo:

Basic structure studies of the biosynthetic machinery of the cell by electron microscopy (EM) have underpinned much of our fundamental knowledge in the areas of molecular cell biology and membrane traffic. Driven by our collective desire to understand how changes in the complex and dynamic structure of this enigmatic organelle relate to its pivotal roles in the cell, the comparatively high-resolution glimpses of the Golgi and other compartments of the secretory pathway offered to us through EM have helped to inspire the development and application of some of our most informative, complimentary (molecular, biochemical and genetic) approaches. Even so, no one has yet even come close to relating the basic molecular mechanisms of transport, through and from the Golgi, to its ultrastructure, to everybody's satisfaction. Over the past decade, EM tomography has afforded new insights into structure -function relationships of the Golgi and provoked a re-evaluation of older paradigms. By providing a set of tools for structurally dissecting cells at high-resolution in three-dimensions (3D), EM tomography has emerged as a method for studying molecular cell biology in situ. As we move rapidly toward the establishment of molecular atlases of organelles through advances in proteomics and genomics, tomographic studies of the Golgi offer the tantalizing possibility that one day, we will be able to map the spatio-temporal coordinates of Golgi-related proteins and lipids accurately in the context of 4D cellular space. (c) 2005 Elsevier B.V. All rights reserved.

Relevância:

10.00% 10.00%

Publicador:

Resumo:

The durability of all forms of open or percutaneous revascularisation is affected by the development of localised stenoses within the bypass graft or at the site of endarterectomy, stent or angioplasty. The reported incidence of significant restenosis has varied dependent on initial procedure, site, case mix and definition, but is greatest during the first 12 months (Table 1).1 Over the last 40 years tens of thousands of studies have been carried out in an effort to understand or reduce the incidence of restenosis, with two major mechanisms identified as being responsible for the luminal narrowing, namely intimal hyperplasia and constrictive remodelling. Intimal hyperplasia is provoked by changes in the balance of local cytokines controlling vascular smooth muscle cell (VSMC) proliferation, apoptosis and migration, brought about by endothelial or medial injury and alterations in haemodynamic forces. The overall vessel diameter reduction that occurs in constrictive remodelling is less well defined, but likely involves matrix turnover under the control of proteinases, particularly metalloproteinases.