30 research outputs found
Sustainability in the existing Dutch Metropolitan office market: Direct and indirect benefits & Conditions for improving the building's level of sustainability
No full textCorporate Real Estate and ManagementReal Estate & HousingArchitectur
Strategic change management toward agile manufacturing : a Hong Kong experience : executive summary
No full textThis paper is the executive summary of the portfolio of the author toward the award of
Engineering Doctorate of the Warwick University. The title of the portfolio is the same as the
title of this paper, which serves as a tool to integrate the works of the author in the whole
portfolio. There are ten other papers in the portfolio besides this one.
The development and implementation of the author's model of Strategic Change Management
(SCM) in a power supply manufacturing company in Hong Kong leading to Agility (AG) is
presented in the paper. SCM developed by the author is a comprehensive and practical model
that a company can use to improve various aspects of its business. The author has demonstrated
this in the areas of Total Quality Management and IS09000 implementation, technology
innovation, supply chain management, renovation of information systems, etc. Three mini
research projects are included in the portfolio, including the development of a What-if prototype
to tackle a common problem in manufacturing resources planning, the design of power supply
products for mass customization, and an empirical study on the factor structures and correlations
of employee job satisfaction (SAT), organisation excellence (EX) and agility (AG).
The SCM model starts with creating the culture for change, which the author sees as the role for
the top management of the organisation. The author presents his experience to create such
culture when he was parachuted into his organisation as the chief executive. The second step of
SCM is analysing the system. A comprehensive qualitative analysis of the economical, social
and cultural environment of the company as well as the market forces is given. The step that
follows is the implementation of changes, which is a cycle of setting priority, organising,
performance measurement, rewarding winners and reinforcement. Practical approaches to tackle
the changes in various stages of the cycle are presented.
SCM has helped in transforming the company toward agility, and the stage of agility is named
Agility Chain by the author. The result of such transformation is also evaluated from the angles
of operations performance, financial performance, stock price appreciation, and the change in
market perception. The empirical study of employees perception on SAT, EX and AG indicates
strong correlations among the three factor structures, and also indicates that the company is
moving toward agility under the author's strategic change management
Risk facing U.S. commercial banks
No full textThe study examines the financial state of the U.S. commercial banks and of the main private borrowing sectors: corporate non-financial business and households. The study finds that the condition of the banks'loan portfolios exposes them to high losses. This risk together with the forthcoming increase of the required ratio of capital to assets suggests that banks will respond by slowing the growth of credit. One consequence would be weaker U.S. investment and consumption. Moreover, credit would probably be directed away from higher risk borrowers such as the highly indebted countries.Financial Crisis Management&Restructuring,Banks&Banking Reform,Financial Intermediation,Economic Theory&Research,International Terrorism&Counterterrorism
Effect of a serotonin blocking agent on renal hemodynamics in the normal rat
No full textEffect of a serotonin blocking agent on renal hemodynamics in the normal rat. These studies were designed to explore the effects of ketanserin (K), a serotonergic S2-receptor blocker on glomerular filtration rate (GFR), renal plasma flow (RPF) and autoregulation of renal blood flow (RBF) in the normal, anesthetized rat. Two doses of ketanserin were used: a high dose that, in addition to its serotonin blocking effect, possessed alpha 1-adrenergic blocking capacities; and a low dose that acted only as a serotonin S2 blocking agent. The effects of the high dose were compared to the effects of phenotolamine. Both the high dose of K and phentolamine resulted in a similar fall of systemic blood pressure from 117 ± 4 to 78 ± 3 and from 121 ± 4.5 to 76 ± 5mm Hg, respectively (P < 0.01). Despite this fall, GFR and RPF remained unchanged from 2.36 ± 0.16 ± to 2.26 ± 0.12 ml/min, and from 5.33 ± 0.41 to 5.76 ± 0.5ml/min with K, while both parameters significantly decreased with phentolamine. A remarkable preservation of the autoregulation of RBF until a renal perfusion pressure (RPP) of 70 to 75mm Hg was noted with K, but not with phentolamine or Ringer infusion. With the low dose of K, a significant rise in GFR and PAH clearance was noted, from 2.12 ± 0.17 to 2.59 ± 0.18 and from 4.81 ± 0.35 to 5.66 ± 0.48 ml/min, respectively (P < 0.05). A similar preservation of autoregulation of RBF was observed. Our studies suggest that in the pressure ranges below normal autoregulation of RBF in the rat, serotonin blockade is associated with maintenance of both GFR and RBF
Lipid alterations induced by renal ischemia: Pathogenic factor in membrane damage
No full textLipid alterations induced by renal ischemia: Pathogenic factor in membrane damage. Lipids of the renal cortex and outer stripe of outer medulla were analyzed in rats during ischemia and 2 hr after blood re-flow. After 15 min of ischemia, there were marked elevations of free fatty acids (FFA) and diacylglycerol (DG), increasing further at 60 min. Percentile increases were greater for polyunsaturated FFA. These elevations were accompanied by alterations in phospholipids (PL): Elevations of lysophosphatidylcholine (LPC) at 15 min, phosphatidic acid at 15 and 60 min, and declines of phosphatidylcholine and phosphatidylinositol at 60 min. Triacylglycerol (TG) showed only modest decline, at 60 min, and in insufficient degree to account for increments in FFA and DG. Two hours after 15 min of ischemia, LPC returned to control levels and other PL were normal except phosphatidylinositol which was decreased, and phosphatidic acid, which remained elevated. FFA and DG approached or reached control values. Two hours after 60 min of ischemia, LPC, FFA, DGs and phosphatidic acid remained elevated; phosphatidylcholine and phosphatidylinositol remained decreased. Histological injury was seen 2 and 24 hr after blood reflow only in kidneys injured by 60 min of ischemia. Thus, irreversible ischemic damage correlates with persistent abnormalities of phosphatidylcholine metabolism and persistent elevations of FFA, LPC, and DG. It is not known whether lipids break down at normal or accelerated rates during ischemia. In this context, accumulation of lipid breakdown products in ischemic cells may be due to failure of their reutilization, or disposal. Similarly, depletion of phospholipids during ischemia may be due to the inability of cells to reconstitute the lipid following degradation. Regardless of the mechanism, the depletion of phospholipids and accumulation of lipid breakdown products which occur during ischemia may be responsible for membrane damage. In partial agreement with this view, the addition of unesterified, unsaturated fatty acids to primary cultures of proximal tubule cells was shown to result in plasma membrane blebbing and cell death.Altérations lipidiques induites par l'ischémie rénale: Un facteur pathogène pour les lésions membranaires. Les lipides de la corticale et de la couche externe de la médullaire externe rénales ont été analysés chez des rats au cours d'une ischémie, et 2 heures après recirculation sanguine. Après 15 minutes d'ischémie, il existait des élévations marquées des acides gras libres (FFA) et du diacylglycérol (DG), qui augmentaient encore à 60 minutes. Les élévations en pourcentage étaient plus fortes pour les FFA polyinsaturés. Ces élévations s'accompagnaient d'altérations des phospholipides (PL): augmentation de la lysophosphatidylcholine (LCP) à 15 minutes, de l'acide phosphatidique à 15 et 60 minutes, et baisses de la phosphatidylcholine et du phosphatidylinositol à 60 minutes. Le triacylglycerol (TG) diminuait seulement modérément à 60 minutes, et de façon insuffisante pour rendre compte des élévations de FFA et de DG. Deux heures après 15 minutes d'ischémie, LPC est retournée aux niveaux contrôles, et les autres PL étaient normaux à l'exception du phosphatidylinositol qui était diminué, et de l'acide phosphatidique qui restait élevé. Les FFA et DG approchaient ou atteignaient les valeurs contrôles. Deux heures après 60 minutes d'ischémie, les LPC, FFA, DGs et l'acide phosphatidique restaient élevés; la phosphatidylcholine et le phosphatidylinositol restaient bas. Des lésions histologiques ont été observées au bout de 2 et 24 heures après recirculation sanguine uniquement dans les reins altérés par 60 minutes d'ischémie. Ainsi, une atteinte ischémique irréversible est corrélée à des anomalies persistantes du métabolisme de la phosphatidylcholine, et à des élévations persistantes des FFA, LPC, et DG. On ne sait pas si les lipides se dégradent à des vitesses normales ou élevées au cours de l'ischémie. Dans ce contexte, l'accumulation de produits de dégradation des lipides dans les cellules ischémiques pourrait résulter d'un trouble de leur réutilisation ou de leur élimination. De même, la depletion en phospholipides lors de l'ischémie pourrait résulter d'une incapacité des cellules à reconstituer les lipides après leur dégradation. Quel qu'en soit le mécanisme, la depletion en phospholipides et l'accumulation de produits de dégradation des lipides qui surviennent pendant l'ischémie pourraient être responsables d'une altération membranaire. En accord partiel avec cette idée, l'addition des les acides gras non estérifiés et non saturés à les cultures primaires des cellules tubulaires proximales a été montré résulter dans de bulles dans la membrane plasmique et la mort des cellules
Alterations in vascular function and morphology in acute ischemic renal failure
No full textAlterations in vascular function and morphology in acute ischemic renal failure. Left renal arteries of rats were clamped for 40 min, and the kidneys were studied 48hr and 7 days following restoration of blood flow. At 48hr, there was severe oliguria or anuria. Renal blood flow (RBF) was in the normal range, but there was a loss of RBF autoregulation between 95 to 120mm of mercury in seven out of nine rats. Morphologically, arcuate and interlobular arteries and afferent arterioles showed focal, segmental necrosis of smooth muscle cells and diapedesis of red blood cells across their walls. At 7 days, renal function was still severely depressed. RBF showed a slight decrease that did not reach statistical significance, and RBF autoregulatory capacity was lost in 8 out of 11 rats. Morphologically, vascular lesions were characterized at this stage by marked thickening and fibrosis of the tunica adventitia of the interlobular arteries and afferent arterioles. Structural vascular alterations may impair smooth muscle contractile function and thus interfere with RBF autoregulatory function in this model of acute renal failure.Altérations de la fonction et de la morphologie vasculaires dans l'insuffisance rénale aiguë ischémique. Les artères rénales gauches de rats ont été clampées pendant 40 min, et les reins étudiés 48hr et 7 jours après la restauration du flux sanguin. A 48hr il y avait une oligurie sévère ou une anurie. Le flux sanguin rénal (RBF) était dans les limites de la normale, mais il y avait une perte de G autorégulation du RBF entre 95 à 120mm Hg chez sept des neuf rats. Morphologiquement, les artères arquées et interlobulaires et les artérioles afférentes avaient une nécrose focale et segmentaire des cellules musculaires lisses, et une diapédèse des globules rouges à travers leurs parois. A 7 jours, la fonction rénale était encore sévèrement altérée. Il existait une diminution modérée du RBF, n'atteignant pas la significativité, et la capacité d'autorégulation du RBF était perdue chez 8 des 11 rats. Morphologiquement, les lésions vasculaires étaient caractérisées à ce stade par un épaississement marqué et une fibrose de la tunique adventitielle des artères interlobulaires et des arterioles afférentes. Les altérations structurelles vasculaires pourraient altérer la fonction contractile mus culaire lisse et interférer ainsi avec la capacité d'autorégulation du RBF dans ce modèle d'insuffisance rénale aiguë
Pseudophaloe promiscua Becker & Espinosa. The 2014
No full textPseudophaloe promiscua Becker & Espino [z]a, 2013 Pseudophaloe promiscua Becker & Espino [z] a, 2013: 63. TYPE LOCALITY. — Costa Rica, Limon, Res[erve] Biol[ogic] Hitoy Cerere. TYPE SPECIMEN. — Holotype male (INBC). REMARK Becker (2013: 54) in the nomenclatural summary of his article, cited “ Pseudophaloe promiscua Becker, sp. n. ”. Becker (2013: 63) described Pseudophaloe promiscua Becker & Espinosa. The holotype is housed in INBC where Bernardo Espinoza is, in particular, a specialist of the Arctiinae. It is obvious that Becker wishes to associate Bernardo Espinoza as co-author of this taxon, despite forgetting his name in the nomenclatural summary and its unfortunate mistake in the emendation surname of Bernardo Espinoza.Published as part of Laguerre, Michel, 2014, Catalogue of the Neotropical Arctiini Leach, [1815] (except Ctenuchina Kirby, 1837 and Euchromiina Butler, 1876) (Insecta, Lepidoptera, Erebidae, Arctiinae), pp. 137-533 in Zoosystema 36 (2) on page 441, DOI: 10.5252/z2014n2a1, http://zenodo.org/record/539534
Heterozygous loss-of-function SEC61A1 mutations cause autosomal-dominant tubulo-interstitial and glomerulocystic kidney disease with anemia
No full textAutosomal-dominant tubulo-interstitial kidney disease (ADTKD) encompasses a group of disorders characterized by renal tubular and interstitial abnormalities, leading to slow progressive loss of kidney function requiring dialysis and kidney transplantation. Mutations in UMOD, MUC1, and REN are responsible for many, but not all, cases of ADTKD. We report on two families with ADTKD and congenital anemia accompanied by either intrauterine growth retardation or neutropenia. Ultrasound and kidney biopsy revealed small dysplastic kidneys with cysts and tubular atrophy with secondary glomerular sclerosis, respectively. Exclusion of known ADTKD genes coupled with linkage analysis, whole-exome sequencing, and targeted re-sequencing identified heterozygous missense variants in SEC61A1-c.553A>G (p.Thr185Ala) and c.200T > G (p.Val67Gly)-both affecting functionally important and conserved residues in SEC61. Both transiently expressed SEC6A1A variants are delocalized to the Golgi, a finding confirmed in a renal biopsy from an affected individual. Suppression or CRISPR-mediated deletions of sec61al2 in zebrafish embryos induced convolution defects of the pronephric tubules but not the pronephric ducts, consistent with the tubular atrophy observed in the affected individuals. Human mRNA encoding either of the two pathogenic alleles failed to rescue this phenotype as opposed to a complete rescue by human wild-type mRNA. Taken together, these findings provide a mechanism by which mutations in SEC61A1 lead to an autosomal-dominant syndromic form of progressive chronic kidney disease. We highlight protein translocation defects across the endoplasmic reticulum membrane, the principal role of the SEC61 complex, as a contributory pathogenic mechanism for ADTKD
