982 resultados para masque nasal


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t. I. La lépreuse. L'holocauste.--t. II. Le masque L'enchantement.--t. III. Résurrection. Maman Colibri.--t. IV. La marche nuptiale. Poliche.--t. V. La femme nue. Le scandale.--t. VI. La vierge folle. Le songe d'un soir d'amour. La déclaration.--VII. Le phalène.--t. VIII. L'enfant de l'amour. Notre image.--t. IX. Les flambeaux. Les soeurs d'amour.--t. X. L'amazone. L'animateur.--t. XI. L'homme à la rose. La tendresse.--t. XII. La possession. La chair humaine.

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Contiene : La papesse Jeanne. L'Inquisition. Galilée, martyr de l'Inquisition. Les rois fainéants. L'usurpation de Hugues Capet. La Saint-Barthélemy. L'Homme au masque de fer. Le père Loriquet. L'Evèque Virgile et les Antipodes.

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v. 1. Demetria. Hadad. Percy's masque.--v. 2. The judgement. Sachem's-wood. Discourses: I. On the choice of an era in epic and tragic writing. II. On the relations of literature to a republican government. III. On the life and services of Lafayette. The hermit of Warkworth, by Bishop Percy.

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The fall of the house of Usher.--The masque of the Red Death.--The pit and the pendulum.--The black cat.--The facts in the case of M. Valdemar.--The gold bug.--The murders in the Rue Morgue.

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v. 1. Introduction. Britannia's pastorals. Books I and II.--v. 2. Britannia's pastorals. Book III. The Shepherd's pipe. The inner Temple masque. Miscellaneous poems. Notes. Index of names.

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Cont. Fair maid of the inn. Cupid's revenge.--v. 10. Two noble kinsmen. Tragedy of Thierry and Theodorey. Woman-hater. Nice valour, or, the passionate madman. Honest man's fortune. Masque. Four plays, or moral representations, in one.

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With reproductions of original title-pages.

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(Vol. 8 translated by Willa and Edwin Muir.)

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Contributions from the Museum of the American Indian, Heye Foundation, vol. 3.

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"Printed for subscriber's only. 450 copies small paper."

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Editors: v. 1, Arnold Glover; v. 2, Arnold Glover and A. R. Waller; v. 3-10, A. R. Waller.

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Includes index.

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Morphine-6beta-D-glucuronide (M6G) is an analgesically active metabolite of morphine, accounting for approximate to10% of the morphine dose when administered by systemic routes to humans. Although M6G is more hydrophilic than morphine, it crosses the blood-brain barrier, albeit relatively slowly. For this reason, it is generally thought that, after chronic dosing, M6G contributes significantly to the analgesic effects of systemically administered morphine. Owing to its polar nature, M6G is cleared from the systemic circulation primarily via renal elimination. As M6G accumulates in patients with renal impairment, there is an increased risk of M6G-induced respiratory depression in renal failure patients who are being dosed chronically with systemic morphine. Consistent with its analgesic and respiratory depressant properties, M6G binds to the p-opioid receptor in a naloxone-reversible manner. Although the affinity of M6G for the mu-opioid receptor is similar to or slightly less than that of morphine, preclinical studies in rodents show that M6G is one to two orders of magnitude more potent than morphine when administered by central routes. This major discrepancy between the markedly higher intrinsic antinociceptive potency of M6G relative to morphine, despite their similar p-opioid receptor binding affinities, is difficult to reconcile. It has been proposed that M6G mediates its pain-relieving effects through a novel 'M6G opioid receptor', while others have argued that M6G may have higher efficacy than morphine for transduction of intracellular events. When administered by parenteral routes to rodents, M6G's antinociceptive potency is no more than twofold higher than morphine. In humans, the analgesic efficacy and respiratory depressant potency of M6G relative to morphine have been assessed in a number of short-term studies involving the intrathecal or intravenous routes of administration. For example, in hip replacement patients, intrathecal M6G provided excellent postoperative analgesia but the occurrence of late respiratory depression in 10% of these patients raised serious concern about safety. In postoperative patients, intravenous M6G administered by means of patient-controlled analgesia (PCA), or bolus plus PCA, produced no analgesia in one study and limited analgesia in another. Similarly, there was a lack of significant analgesia in healthy volunteers who received intravenous M6G for the alleviation of experimental pain (carbon dioxide applied to the nasal mucosa). In contrast, satisfactory analgesia was produced by bolus doses of intravenous M6G administered to patients with cancer pain, and to healthy volunteers with experimentally-induced ischaemic, electrical or thermal (ice water) pain. Studies to date in healthy volunteers suggest that intravenous M6G may be a less potent respiratory depressant and have a lower propensity for producing nausea and vomiting than morphine. However, it is unclear whether equi-analgesic doses of M6G and morphine were compared. Clearly, more extensive short-term trials, together with studies involving chronic M6G administration, are necessary before the potential clinical utility of M6G as an analgesic drug in its own right can be determined.

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Trafficking of the cystic fibrosis transmembrane conductance regulator (CFTR) is central to its function, with the most common mutation, DeltaF508, resulting in abnormal processing and trafficking. Therefore, there is a significant need to develop tools, which enable the trafficking of CFTR to be studied in vitro and in vivo. In previous studies it has been demonstrated that fusion of the green fluorescent protein (GFP) to the N-terminus of CFTR does lead to functional expression of CFTR chloride channels in epithelial cell lines. The aim of the present study was to examine whether it is possible to express GFP-tagged CFTR as a transgene in colonic and airway epithelial cells of cystic fibrosis (CF) mice and to correct the CF defect. Using the epithelial-specific human cytokeratin promoter K18, we generated bitransgenic mice cftr(G551D/G551D) K18-GFP-CFTR+/-, designated GFP mice. Transcripts for GFP-CFTR could be detected in bitransgenic mice by use of RT-PCR techniques. Expression of GFP-CFTR protein was detected specifically in the colonic epithelium by both direct GFP fluorescence and the use of an anti-GFP antibody. Ussing chamber studies showed that the ion transport defect in colon and airways observed in cftr(G551D/G551D) mice was partially corrected in the bitransgenic animals. Thus, K18-GFP-CFTR is functionally expressed in transgenic mice, which will be a valuable tool in studies on CFTR synthesis, processing and ion transport in native epithelial tissues.