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General Loss (general + loss)
Selected AbstractsDiversity, distinctiveness and conservation status of the Mediterranean coastal dung beetle assemblage in the Regional Natural Park of the Camargue (France)DIVERSITY AND DISTRIBUTIONS, Issue 6 2001Jorge Miguel Lobo Abstract. The Mediterranean region as a whole has the highest dung beetle species richness within Europe. Natural coastal habitats in this region are among those which have suffered severe human disturbance. We studied dung beetle diversity and distinctiveness within one of the most important coastal protected areas in the west Euro-Mediterranean region (the regional Park of Camargue, southern France) and made comparisons of dung beetle assemblages with other nearby Mediterranean localities, as well as with other coastal protected area (Doñana National Park, Spain). Our finding showed that: (1) The species richness of coastal habitats in the Camargue is low and only grasslands showed a similar level of species richness and abundance to inland habitats of other Mediterranean localities. The unique habitats of the coastal area (beaches, dunes and marshes) are largely colonized by species widely distributed in the hinterland. (2) In spite of their low general distinctiveness, dune and marsh edges are characterized by the occurrence of two rare, vulnerable, specialized and large roller dung beetle species of the genus Scarabaeus. As with other Mediterranean localities, current findings suggest a recent decline of Scarabaeus populations and the general loss of coastal dung beetle communities in Camargue. (3) The comparison of dung beetle assemblages between the Camargue and Doñana shows that, in spite of the low local dung beetle species richness in the Camargue, the regional dung beetle diversity is similar between both protected areas. Unique historical and geographical factors can explain the convergence in regional diversity as well as the striking divergence in the composition of dung beetle assemblages between both territories. [source] Characterization of Neuronal Migration Disorders in Neocortical Structures: Loss or Preservation of Inhibitory Interneurons?EPILEPSIA, Issue 7 2000Petra Schwarz Summary: Purpose: Neuronal migration disorders (NMD) are often associated with therapy-resistant epilepsy. In human cerebral cortex, this hyperexcitability has been correlated with a loss of inhibitory interneurons. We used a rat model of focal cortical NMD (microgyria) to determine whether the expression of epileptiform activity in this model coincides with a decrease in inhibitory interneurons. Methods: In 2- to 4-month-old rats, the density of interneurons immunoreactive for ,-aminobutyric acid (GABA), cal-bindin, and parvalbumin was determined in fronto-parietal cortex in nine 200-,m-wide sectors located up to 2.5 mm lateral and 2.0 mm medial from the lesion center in primary parietal cortex (Par 1). Quantitative measurements in homotopic areas of age-matched sham-operated rats served as controls. Results: The freeze lesion performed in newborn rat cortex resulted in adult rats with a microgyrus extending in a rostro-caudal direction from frontal to occipital cortex. The density of GABA- and parvalbumin-positive neurons in fronto-parietal cortex was not significantly different between lesioned and control animals. Only the density of calbindin-immunoreactive neurons located 1.0 mm lateral and 0.5 mm medial from the lesion was significantly (Student t test, p > 0.05) larger in freeze-lesioned rats (5.817 ± 562 and 6,400 ± 795 cells per mm3, respectively; n = 12) compared with measurements in homotopic regions in Parl cortex of controls (4,507 ± 281 and 4,061 ± 319 cells per mm3, respectively; n = 5). Conclusions: The previously reported widespread functional changes in this model of cortical NMD are not related to a general loss of inhibitory interneurons. Other factors, such as a decrease in GABA receptor density, modifications in GABAA receptor subunit composition, or alterations in the excitatory network, e.g., an increase in the density of calbindin-immunoreactive pyramidal cells, more likely contribute to the global disinhibition and widespread expression of pathophysiological activity in this model of cortical NMD. [source] Down-regulation of reduced folate carrier may result in folate malabsorption across intestinal brush border membrane during experimental alcoholismFEBS JOURNAL, Issue 24 2007Abid Hamid Folate plays a critical role in maintaining normal metabolic, energy, differentiation and growth status of all mammalian cells. The intestinal folate uptake is tightly and diversely regulated, and disturbances in folate homeostasis are observed in alcoholism, attributable, in part, to intestinal malabsorption of folate. The aim of this study was to delineate the regulatory mechanisms of folate transport in intestinal absorptive epithelia in order to obtain insights into folate malabsorption in a rat model of alcoholism. The rats were fed 1 g·kg,1 body weight of ethanol daily for 3 months. A reduced uptake of [3H]folic acid in intestinal brush border membrane was observed over the course of ethanol administration for 3 months. Folate transport exhibited saturable kinetics and the decreased intestinal brush border membrane folate transport in chronic alcoholism was associated with an increased Km value and a low Vmax value. Importantly, the lower intestinal [3H]folic acid uptake in ethanol-fed rats was observed in all cell fractions corresponding to villus tip, mid-villus and crypt base. RT-PCR analysis for reduced folate carrier, the major folate transporter, revealed that reduced folate carrier mRNA levels were decreased in jejunal tissue derived from ethanol-fed rats. Parallel changes were observed in reduced folate carrier protein levels in brush border membrane along the entire crypt,villus axis. In addition, immunohistochemical staining for reduced folate carrier protein showed that, in alcoholic conditions, deranged reduced folate carrier localization was observed along the entire crypt,villus axis, with a more prominent effect in differentiating crypt base stem cells. These changes in functional activity of the membrane transport system were not caused by a general loss of intestinal architecture, and hence can be attributed to the specific effect of ethanol ingestion on the folate transport system. The low folate uptake activity observed in ethanol-fed rats was found to be associated with decreased serum and red blood cell folate levels, which might explain the observed jejunal genomic hypomethylation. These findings offer possible mechanistic insights into folate malabsorption during alcoholism. [source] Loss of SNAP-25 and rabphilin 3a in sensory-motor cortex in Huntington's diseaseJOURNAL OF NEUROCHEMISTRY, Issue 1 2007Ruben Smith Abstract Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder caused by a CAG-expansion in the gene encoding the protein huntingtin. The disease is characterized by progressive motor disturbances, cognitive defects, dementia, and weight loss. Using western blotting and immunohistochemistry we have assessed the expression levels and patterns of a number of proteins involved in neurotransmitter release in post-mortem frontal cortex samples from 10 HD cases with different disease grades. We report a loss of the soluble N -ethylmaleimide-sensitive factor attachment protein receptor (SNARE) protein, synaptosome-associated protein 25 (SNAP 25) in HD brains of grades I,IV. Moreover, in brains of grade III and IV we found a reduction in rabphilin 3a, a protein involved in vesicle docking and recycling. These losses appear to be specific and not due to a general loss of synapses in the HD cortex. Thus, levels of synaptobrevin II, syntaxin 1, rab3a or synaptophysin are unaltered in the same patient samples. SNAP 25 and rabphilin 3a are crucial for neurotransmitter release. Therefore, we suggest that a deficient pre-synaptic transmitter release may underlie some of the symptoms of HD. [source] Transplanted dopaminergic neurons develop PD pathologic changes: A second case report,MOVEMENT DISORDERS, Issue 16 2008Jeffrey H. Kordower PhD Abstract This report describes pathological changes within the grafted neurons of another patient with Parkinson's disease (PD) who died 14 years posttransplantation. Although numerous healthy appearing grafted neurons were present at this long-term time point, some displayed Lewy bodies as evidenced by alpha-synuclein, ubiquitin, and thioflavin-S staining. Additionally, there was a general loss of dopamine transporter-immunoreactivity in grafted neurons. Some grafted cell displayed a loss of tyrosine hydroxylase. These data support the emerging concept that PD-like pathology is seen in young grafted neurons when they survive long term. © 2008 Movement Disorder Society [source] Temperature-dependent structural changes in intrinsically disordered proteins: Formation of ,,helices or loss of polyproline II?PROTEIN SCIENCE, Issue 8 2010Magnus Kjaergaard Abstract Structural characterization of intrinsically disordered proteins (IDPs) is mandatory for deciphering their potential unique physical and biological properties. A large number of circular dichroism (CD) studies have demonstrated that a structural change takes place in IDPs with increasing temperature, which most likely reflects formation of transient ,,helices or loss of polyproline II (PPII) content. Using three IDPs, ACTR, NHE1, and Spd1, we show that the temperature-induced structural change is common among IDPs and is accompanied by a contraction of the conformational ensemble. This phenomenon was explored at residue resolution by multidimensional NMR spectroscopy. Intrinsic chemical shift referencing allowed us to identify regions of transiently formed helices and their temperature-dependent changes in helicity. All helical regions were found to lose rather than gain helical structures with increasing temperature, and accordingly these were not responsible for the change in the CD spectra. In contrast, the nonhelical regions exhibited a general temperature-dependent structural change that was independent of long-range interactions. The temperature-dependent CD spectroscopic signature of IDPs that has been amply documented can be rationalized to represent redistribution of the statistical coil involving a general loss of PPII conformations. [source] Health-care reform and the dimensions of professional autonomyCANADIAN PUBLIC ADMINISTRATION/ADMINISTRATION PUBLIQUE DU CANADA, Issue 1 2009Glen E. Randall With this model, it was assumed that competitive forces would encourage quality while driving down costs. While such reforms often achieve cost controls by constraining the incomes and practices of health-care workers, there has been relatively little analysis of the extent to which self-governing health-care professionals, particularly those outside of medicine and nursing, may experience a decline in their ability to control the content and context of their professional work. In this article, the authors analyse the results of thirty-six in-depth interviews with representatives of Community Care Access Centres (CCACs), the organizations that purchase and coordinate the delivery of home-care services, and rehabilitation provider agencies to examine the impact of Ontario's managed competition reform on rehabilitation professionals. Findings suggest that the impact of the reform varied across the economic, political, and clinical dimensions of professional autonomy and that, despite a general loss of autonomy under the managed competition model, market forces also served to mitigate the loss of autonomy, thus contributing to a remarkable resilience of professional autonomy. Sommaire: Un modèle de « concurrence dirigée » a été introduit récemment dans la province canadienne de l'Ontario dans le cadre de la réforme gouvernementale des soins à domicile. Avec ce modèle, il était présumé que les forces de la concurrence encourageraient la qualité tout en faisant baisser les coûts. Alors que de telles réformes parviennent souvent à maîtriser les coûts en réduisant les revenus et les pratiques des travailleurs de la santé, il y a eu relativement peu d'analyses de faites sur la mesure dans laquelle les professionnels de la santé autonomes, particulièrement ceux qui exercent en dehors de la médecine et de la profession infirmière, connaissent une perte de contrôle sur le contenu et le contexte de leur travail professionnel. Dans le présent article, les auteurs analysent les résultats de trente-six entrevues en profondeur menées auprès de représentants des Centres d'accès aux soins communautaires (CASC), organismes qui achètent et coordonnent la prestation des services de soins à domicile, et organismes de prestation de soins de réadaptation, afin d'examiner les conséquences de la réforme de la concurrence dirigée de l'Ontario sur les professionnels de la réadaptation. Les résultats laissent entendre que l'effet de la réforme a varié en fonction des dimensions économiques, politiques et cliniques de l'autonomie professionnelle et que, malgré une perte d'autonomie générale liée au modèle de concurrence dirigée, les forces du marché ont également permis d'atténuer la perte d'autonomie, contribuant ainsi à la remarquable résilience dont font preuve ces professionnels en la matiére. [source] | ||||||||||||||||