			Home About us Contact

Structural Deficits (structural + deficit)

Distribution by Scientific Domains

Medical Sciences	50%

Selected Abstracts

Constraints to Drought Contingency Planning in Spain: The Hydraulic Paradigm and the Case of Seville

JOURNAL OF CONTINGENCIES AND CRISIS MANAGEMENT, Issue 2 2000
Leandro Del Moral Ituarte
Spain is equipped with an extensive hydraulic infrastructure, aimed at the correction of temporal and spatial irregularities in the availability of water resources. This structural network, mainly based on surface water, is the manifestation of the traditional hydraulic paradigm, which has technical, economic, socio-political and cultural ramifications. The traditional water management perspective tends to view drought as the structural deficit between water demand and water regulation capacity. This conceptualisation of drought led primarily to a structural response, while ignoring the need for drought risk assessment and water crisis management rules. The traditional hydraulic paradigm can, paradoxically, be regarded as one of the main constraints to the development of drought contingency planning and drought management. However, a new dynamism has entered the water policy arena, which encompasses elements of both innovation and persistence of the traditional perception. This dynamism is analysed through the Seville water management system, which is often affected by drought and severe water crises. [source]

PAIN REDUCTION WITH OPIOID ELIMINATION

PAIN MEDICINE, Issue 2 2002
Article first published online: 4 JUL 200
Edward Covington, MD, Cleveland Clinic Foundation; Margaret Kotz, DO, Cleveland Clinic Foundation The last decade has seen a reversal of the historical belief that chronic opioid therapy (COT) was inadvisable in nonmalignant palm. Numerous studies demonstrate sustained pain reduction with chronic opioid therapy; however, there are clinical reports and animal models that suggest chronic opioids may at times exacerbate pain. Clearly, many patients without apparent structural deficit have persistent pain and dysfunction despite high dose opioid therapy. Thus, while opioids have been shown to be safe in long term use, the question of efficacy remains. Predictors of success in COT are not fully established. Studies of intrathecal opioids suggest that high levels of patient satisfaction and retrospective reports of benefit may occur despite minimal change in pain level and function. This raises the question of whether at times the purported benefits of long-term opioid therapy may be illusory. Consecutive admissions to a chronic pain rehabilitation program (n = 228) were studied. This program represents a biased population in that many referrals have dysfunction that is discordant with pathology, inordinate suffering and dysphoria, poorly explained pain, or substance use problems. Of 228, 56 were taking , 100 mg p.o. morphine equivalents/d on admission (mean 456 mg/d). Data are available on 46 of these receiving ,high dose' opioids. Patients participated in a rehabilitation program that included reconditioning, cognitive behavioral psychotherapy, adjuvant medications, and elimination of opioids and benzodiazepines. 43 (93%) experienced a reduction in pain with opioid elimination (from 7.2 to 4.0/10). Three experienced an increase in pain. Depression and functional impairment also improved. Cases will be presented of patients who believed they were benefiting from chronic opioid therapy, but improved after opioid elimination. They commonly described "getting myself back" after elimination of opioids. Physiological considerations and treatment implications will be described. [source]

Correlation of anatomy and function in medulla oblongata infarction

EUROPEAN JOURNAL OF NEUROLOGY, Issue 2 2009
C. Eggers
Background:, A presentation of all aspects of the dorsolateral medulla oblongata syndrome is clinically very rare to find. In most cases patients present with fragmentary symptoms, e.g. ipsilateral axial lateropulsion, nystagmus, dysarthria, dysphagia or hemiataxia. However, the clinical presentation and lesion anatomy at the level of the medulla oblongata is still unsatisfactory. The aim of this study was to correlate the functional deficit with structural MRI-data. Methods:, We included thirteen patients (eight male, five female, mean age 65.5) with medulla oblongata infarction with clinically predominant ipsilateral axial lateropulsion and correlated clinical with structural deficits. Results:, Magnetic resonance imaging lesion mapping demonstrated ipsilateral axial lateropulsion to result from lesions of the spinocerebellar tract, the inferior cerebellar peduncle or the inferior vestibular nucleus. Nystagmus was associated with lesions of the inferior vestibular nucleus, dissociated sensory loss with the spinothalamic tract and hemiataxia with the spinocerebellar tract. Conclusions:, Correlating dysfunction and lesion anatomy is a promising approach to enhance our knowledge on medulla oblongata topography. [source]

Oligodendrocyte-specific ceramide galactosyltransferase (CGT) expression phenotypically rescues CGT-deficient mice and demonstrates that CGT activity does not limit brain galactosylceramide level

GLIA, Issue 3 2005
Inge Zöller
Abstract Galactosylceramide (GalC) is the major sphingolipid of the myelin membrane. Mice lacking GalC due to ceramide galactosyltransferase (CGT) deficiency form unstable and functionally affected myelin and exhibit a progressive demyelination, accompanied by severe motor coordination deficits. In addition to oligodendrocytes, CGT is also expressed in other cells, e.g., neurons and astrocytes. We examined the possibility that lack of CGT in these cells contributes to the phenotype of CGT-deficient mice. Toward this aim, we generated transgenic mice expressing CGT under the control of oligodendrocyte-specific proteolipid protein (PLP) promoter and examined the possibility of a transgenic rescue of CGT-deficient mice. CGT-deficient mice expressing the PLP-CGT transgene did not show any behavioral abnormalities, normal myelin structure, and MBP levels. CGT activity as well as GalC and sulfatide levels of rescued mice were not significantly different from wild-type controls. Thus, transgenic rescue with the PLP-CGT transgene was apparently complete. In contrast to wild-type and rescued mice, PLP-CGT transgenic mice on a wild-type background exhibited significantly elevated CGT activity which directly correlated with an increase in non-hydroxy fatty acid (NFA)-GalC, but not ,-hydroxy fatty acid (HFA)-GalC. HFA-GalC decreased in adult transgenic mice, indicating that NFA-GalC, but not HFA-GalC levels are limited by CGT activity. As a consequence, the total amount of GalC is unchanged over a rather wide range of CGT expression levels in the mouse brain. Our results indicate that loss of CGT in oligodendrocytes is exclusively responsible for the myelin structural deficits, demyelination, and behavioral abnormalities in CGT-deficient mice. © 2005 Wiley-Liss, Inc. [source]

U.S. Grand Strategy Following the George W. Bush Presidency

INTERNATIONAL STUDIES PERSPECTIVES, Issue 4 2009
David C. Ellis
Debates over U.S. grand strategy have devoted a disproportionate level of attention to the War on Terror itself rather than the evolving strategic environment. Challenges including an impending shift in the balance of power, structural deficits, and divided public opinion will significantly impact the policy options available to government leaders, but they have not been adequately addressed. This article analyzes the options available for U.S. grand strategy following the George W. Bush presidency by relating key U.S. national interests with domestic and international policy constraints on the horizon. The analysis concludes that the United States must adopt a defensive grand strategy to rebuild popular consensus, to prevent further strain on the military, and to consolidate its gains in Iraq and Afghanistan. However, this strategy will require flexible coalitions, not formal international organizations, because of a significant divergence of security interests and capabilities with its European allies. [source]

Apoptosis-inducing factor deficiency sensitizes dopaminergic neurons to parkinsonian neurotoxins

ANNALS OF NEUROLOGY, Issue 2 2010
Celine Perier PhD
Objective Mitochondrial complex I deficits have long been associated with Parkinson disease (PD). However, it remains unknown whether such defects represent a primary event in dopaminergic neurodegeneration. Methods Apoptosis-inducing factor (AIF) is a mitochondrial protein that, independently of its proapoptotic properties, plays an essential physiologic role in maintaining a fully functional complex I. We used AIF-deficient harlequin (Hq) mice, which exhibit structural deficits in assembled complex I, to determine whether primary complex I defects linked to AIF depletion may cause dopaminergic neurodegeneration. Results Despite marked reductions in mitochondrial complex I protein levels, Hq mice did not display apparent alterations in the dopaminergic nigrostriatal system. However, these animals were much more susceptible to exogenous parkinsonian complex I inhibitors, such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Subtoxic doses of MPTP, unable to cause damage to wild-type animals, produced marked nigrostriatal dopaminergic degeneration in Hq mice. This effect was associated with exacerbated complex I inhibition and increased production of mitochondrial-derived reactive oxygen species (ROS) in Hq brain mitochondria. The antioxidant superoxide dismutase-mimetic compound tempol was able to reverse the increased susceptibility of Hq mice to MPTP. Supporting an instrumental role for mitochondrial-derived ROS in PD-related neurodegeneration, transgenic mice overexpressing mitochondrially targeted catalase exhibited an attenuation of MPTP-induced mitochondrial ROS and dopaminergic cell death. Interpretation Structural complex I alterations linked to AIF deficiency do not cause dopaminergic neurodegeneration but increase the susceptibility of dopaminergic neurons to exogenous parkinsonian neurotoxins, reinforcing the concept that genetic and environmental factors may interact in a common molecular pathway to trigger PD. ANN NEUROL 2010;68:184,192 [source]