112 resultados para Wilkie, Gordon
Resumo:
Depending on the size and shape of the materials, methods employed to achieve effective fluidization during fluid bed drying varies from use of simple hole distributors for small, light weight materials to special techniques for lager and/or moist materials. This paper reviews common air distributors used in fluidized bed drying of food particulates. Also it reviews special methods of fluidizing larger irregular food particulates.
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In familial hyperaldosteronism type I (FH-I), inheritance of a hybrid 11 beta-hydroxylase/aldosterone synthase gene causes ACTH-regulated aldosterone overproduction. In an attempt to understand the marked variability in hypertension severity in FH-I, we compared clinical and biochemical characteristics of 9 affected individuals with mild hypertension (normotensive or onset of hypertension after 15 yr, blood pressure never >160/100 mm Hg, less than or equal to 1 medication required to control hypertension, no history of stroke, age >18 yr when studied) with those of 17 subjects with severe hypertension (onset before 15 yr, or systolic blood pressure >180 mm Hg or diastolic blood pressure >120 mm Hg at least once, or greater than or equal to 2 medications, or history of stroke). Severe hypertension was more frequent in males (11 of 13 males vs. 6 of 13 females; P
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The survival, development and feeding responses of Helicoverpa armigera (Hubner) on neem (Azadirachta indica A. Juss) leaflets were evaluated under choice and no-choice conditions. Neem leaflets provided to starving fourth-instar larvae were chewed, but larvae expectorated most of the material. The weight of surviving larvae decreased and no fourth instars completed development on neem leaflets alone. Larvae resumed feeding when transferred to cotton leaves after 5 days of feeding on neem leaflets. Fourth instars strongly discriminated between neem leaflets and cotton leaves when offered a choice. Early sixth instars decreased in weight and had delayed development when feet only on neem leaflets. Mure than one-half lived for more than 2 weeks and some completed development to adults. Neem is an unacceptable non-host plant species for H. armigera.
Resumo:
Familial hyperaldosteronism type II (FH-II) is caused by adrenocortical hyperplasia or aldosteronoma or both and is frequently transmitted in an autosomal dominant fashion. Unlike FH type I (FI-I-I), which results from fusion of the CYP11B1 and CYP11B2 genes, hyperaldosteronism in FH-II is not glucocorticoid remediable. A large family with FH-II was used for a genome wide search and its members were evaluated by measuring the aldosterone:renin ratio. In those with an increased ratio, FH-II was confirmed by fludrocortisone suppression testing. After excluding most of the genome, genetic linkage was identified with a maximum two point lod score of 3.26 at theta =0, between FH-II in this family and the polymorphic markers D7S511, D7S517, and GATA24F03 on chromosome 7,a region that corresponds to cytogenetic band 7p22. This is the first identified locus for FH-II; its molecular elucidation may provide further insight into the aetiology of primary aldosteronism.
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Pheochromocytomas are tumors of the adrenal medulla originating in the chromaffin cells derived from the neural crest. Ten % of these tumors are associated with the familial cancer syndromes multiple endocrine neoplasia type 2, von Hippel-Lindau disease (VHL), and rarely, neurofibromatosis type 1, in which germ-line mutations have been identified in RET, VHL, and NF1, respectively. In both the sporadic and familial forms of pheochromocytoma, allelic loss at 1p, 3p, 17p, and 22q has been reported, yet the molecular pathogenesis of these tumors is largely unknown. Allelic loss at chromosome 1p has also been reported in other endocrine tumors, such as medullary thyroid cancer and tumors of the parathyroid gland, as well as in tumors of neural crest origin including neuroblastoma and malignant melanoma, In this study, we performed fine structure mapping of deletions at chromosome 1p in familial and sporadic pheochromocytomas to identify discrete regions likely housing tumor suppressor genes involved in the development of these tumors. Ten microsatellite markers spanning a region of similar to 70 cM (Ipter to 1p34.3) were used to screen 20 pheochromocytomas from 19 unrelated patients for loss of heterozygosity (LOH). LOH was detected at five or more loci in 8 of 13 (61%)sporadic samples and at five or more loci in four of five (80%) tumor samples from patients with multiple endocrine neoplasia type 2. No LOH at 1p was detected in pheochromocytomas from two VHL patients, Analysis of the combined sporadic and familial tumor data suggested three possible regions of common somatic loss, designated as PCI (D1S243 to D1S244), PC2 (D1S228 to D1S507), and PC3 (D1S507 toward the centromere). We propose that chromosome Ip may be the site of at least three putative tumor suppressor loci involved in the tumorigenesis of pheochromocytomas. At least one of these loci, PC2 spanning an interval of <3.8 cM, is Likely to have a broader role in the development of endocrine malignancies.
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The origin of smooth muscle cells involved in vascular healing was examined. Eighteen C57BL/6 (Ly 5.2) female mice underwent whole body irradiation followed by transfusion with 10(6) bone nucleated marrow cells from congenic (Ly 5.1) male donors. Successful repopulation by donor marrow was demonstrated after 4 weeks by flow cytometry with FITC-conjugated A20.1/Ly 5.1 monoclonal antibody. The iliac artery of six of the chimeric mice was scratch-injured by five passes of a probe, causing severe medial damage. After 4 weeks the arterial lumen was obliterated by a cell-rich neointima, with alpha-smooth muscle actin-containing cells present around the residual lumen. Approximately half of these cells were of male donor origin, as evidenced by in situ hybridization with a Y chromosome-specific probe. An organized arterial thrombus was formed in the remaining 12 chimeric mice by inserting an 8.0 silk suture into the left common carotid artery. Donor cells staining with alpha-smooth muscle actin were found in those arteries sustaining serious damage but not in arteries with minimal damage. Our results suggest that bone marrow-derived cells are recruited in vascular healing as a complementary source of smooth muscle-like cells when the media is severely damaged and few resident smooth muscle cells are available to effect repair.
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Percutaneous transluminal coronary angioplasty is a frequently used interventional technique to reopen arteries that have narrowed because of atherosclerosis. Restenosis, or renarrowing of the artery shortly after angioplasty, is a major limitation to the success of the procedure and is due mainly to smooth muscle cell accumulation in the artery wall at the site of balloon injury. In the present study, we demonstrate that the antiangiogenic sulfated oligosaccharide, PI-88, inhibits primary vascular smooth muscle cell proliferation and reduces intimal thickening 14 days after balloon angioplasty of rat and rabbit arteries. PI-88 reduced heparan sulfate content in the injured artery wall and prevented change in smooth muscle phenotype. However, the mechanism of PI-88 inhibition was not merely confined to the antiheparanase activity of this compound. PI-88 blocked extracellular signal-regulated kinase-1/2 (ERK1/2) activity within minutes of smooth muscle cell injury. It facilitated FGF-2 release from uninjured smooth muscle cells in vitro, and super-released FGF-2 after injury while inhibiting ERK1/2 activation. PI-88 inhibited the decrease in levels of FGF-2 protein in the rat artery wall within 8 minutes of injury. PI-88 also blocked injury-inducible ERK phosphorylation, without altering the clotting time in these animals. Optical biosensor studies revealed that PI-88 potently inhibited (K-i 10.3 nmol/L) the interaction of FGF-2 with heparan sulfate. These findings show for the first time the capacity of this sulfated oligosaccharide to directly bind FGF-2, block cellular signaling and proliferation in vitro, and inhibit injury-induced smooth muscle cell hyperplasia in two animal models. As such, this study demonstrates a new role for PI-88 as an inhibitor of intimal thickening after balloon angioplasty. The full text of this article is available online at http://www.circresaha.org.
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We obtain a class of non-diagonal solutions of the reflection equation for the trigonometric A(n-1)((1)) vertex model. The solutions can be expressed in terms of intertwinner matrix and its inverse, which intertwine two trigonometric R-matrices. In addition to a discrete (positive integer) parameter l, 1 less than or equal to l less than or equal to n, the solution contains n + 2 continuous boundary parameters.
Resumo:
Despite extensive research in the last 150 years, the regional tectonic reconstruction of the Western Alps has remained controversial. The curved orogenic belt consists of several ribbon-like continental terranes (Sesia/Austroalpine, Internal Crystalline Massifs, Brianconnais), which are separated by two or more ophiolitic sutures (Piemonte, Valais, Antrona?, Lanzo/ Canavese?). High-pressure (HP) metamorphism of each terrane occurred during distinct orogenic episodes: at similar to65 Ma in the Sesia/Austroalpine, at similar to45 Ma in the Piemonte zone and at similar to35 Ma in the Internal Crystalline Massifs. It is suggested that these events reflect individual accretionary episodes, which together with kinematic indicators and the speed and direction of plate motions, provide constraints for the discussed reconstruction model. The model involves a prolonged orogenic history that took place during relative convergence of Europe and Adria (here considered as a promontory of the African plate). The first accretionary event involved the Sesia/Austroalpine terrane. Final closure of the Piemonte Ocean occurred during the Eocene (similar to45 Ma) and involved ultra-high-pressure (UHP) metamorphism of the Piemonte oceanic crust. Incorporation of the Brianconnais terrane in the accretionary wedge occurred thereafter, possibly during or after subduction of the Valais Ocean in the late Eocene (45-35 Ma). This subduction was terminated at ca. 35 Ma, when the Internal Crystalline Massifs (i.e. the assumed internal parts of the Brianconnais terrane) were buried into great depths and underwent HP and UHP metamorphism. (C) 2004 Elsevier B.V. All rights reserved.