Home About us Contact
|
Home About us Contact | ||
|
|
||
Decreased Recruitment (decreased + recruitment)
Selected AbstractsWolves, trophic cascades, and rivers in the Olympic National Park, USAECOHYDROLOGY, Issue 2 2008Robert L. Beschta Abstract Gray wolves (Canis lupus) were extirpated in the early 1900s from the Olympic Peninsula of northwestern Washington. Thus, we studied potential cascading effects of wolf removal by undertaking a retrospective study of Roosevelt elk (Cervus elaphus) populations, riparian forests, and river channel morphology. For three riparian sites within the western portion of Olympic National Park, the age structure of black cottonwood and bigleaf maple indicated a pattern of significantly decreased recruitment (growth of seedlings/sprouts into tall saplings and trees) associated with intensive elk browsing in the decades following the loss of wolves. At a riparian site outside the park, which represented a refugium from elk browsing, cottonwood recruitment has been ongoing during the 20th century, indicating that climate and flow regimes, in the absence of intensive herbivory, have not limited the establishment and growth of this deciduous woody species. Using 1994 orthophotos, we also measured channel dimensions and planform morphology of 8-km-long river reaches at each vegetation sampling site and an additional reach outside the park. Channels inside the park versus those outside the park had greater percent braiding (37 vs 2%) and larger ratios of active channel width/wetted width (3·0 vs 1·5 m/m). Results for western Olympic National Park were consistent with a truncated trophic cascade hypothesis whereby ungulate browsing following the extirpation of wolves caused significant long-term impacts to riparian plant communities which, in turn, allowed increased riverbank erosion and channel widening to occur. Copyright © 2008 John Wiley & Sons, Ltd. [source] Sensorimotor network rewiring in mild cognitive impairment and Alzheimer's diseaseHUMAN BRAIN MAPPING, Issue 4 2010Federica Agosta Abstract This study aimed at elucidating whether (a) brain areas associated with motor function show a change in functional magnetic resonance imaging (fMRI) signal in amnestic mild cognitive impairment (aMCI) and Alzheimer's disease (AD), (b) such change is linear over the course of the disease, and (c) fMRI changes in aMCI and AD are driven by hippocampal atrophy, or, conversely, reflect a nonspecific neuronal network rewiring generically associated to brain tissue damage. FMRI during the performance of a simple motor task with the dominant right-hand, and structural MRI (i.e., dual-echo, 3D T1-weighted, and diffusion tensor [DT] MRI sequences) were acquired from 10 AD patients, 15 aMCI patients, and 11 healthy controls. During the simple-motor task, aMCI patients had decreased recruitment of the left (L) inferior frontal gyrus compared to controls, while they showed increased recruitment of L postcentral gyrus and head of L caudate nucleus, and decreased activation of the cingulum compared with AD patients. Effective connectivity was altered between primary sensorimotor cortices (SMC) in aMCI patients vs. controls, and between L SMC, head of L caudate nucleus, and cingulum in AD vs. aMCI patients. Altered fMRI activations and connections were correlated with the hippocampal atrophy in aMCI and with the overall GM microstructural damage in AD. Motor-associated functional cortical changes in aMCI and AD mirror fMRI changes of the cognitive network, suggesting the occurrence of a widespread brain rewiring with increasing structural damage rather than a specific response of cognitive network. Hum Brain Mapp, 2010. © 2009 Wiley-Liss, Inc. [source] Cyclic GMP phosphodiesterase inhibition alters the glial inflammatory response, reduces oxidative stress and cell death and increases angiogenesis following focal brain injuryJOURNAL OF NEUROCHEMISTRY, Issue 3 2010Paula Pifarré J. Neurochem. (2010) 112, 807,817. Abstract Recent evidence obtained in cultured glial cells indicates that cGMP-mediated pathways regulate cytoskeleton dynamics, glial fibrillary acidic protein expression and motility in astrocytes, as well as inflammatory gene expression in microglia, suggesting a role in the regulation of the glial reactive phenotype. The aim of this work was to examine if cGMP regulates the glial inflammatory response in vivo following CNS damage caused by a focal cryolesion onto the cortex in rats. Results show that treatment with the cGMP phosphodiesterase inhibitor zaprinast (10 mg/kg i.p.) 2 h before and 24 and 48 h after the lesion results 3 days post-lesion in notably enhanced astrogliosis manifested by increased glial fibrillary acidic protein immunoreactivity and protein levels around the lesion. In contrast, zaprinast decreased the number of round/ameboid lectin-positive cells and the expression of the activated microglia/macrophage markers Iba-1 and CD11b indicating decreased recruitment and activation of these cells. This altered inflammatory response is accompanied by a decrease in protein oxidative stress, apoptotic cell death and neuronal degeneration. In addition, zaprinast enhanced angiogenesis in the lesioned cortex probably as a result of vascular endothelial growth factor expression in reactive astrocytes. These results suggest that regulation of the glial inflammatory response may contribute to the reported neuroprotective effects of cGMP-phosphodiesterase inhibitors in brain injury. [source] Smoke Exposure and Ethanol Ingestion Modulate Intrapulmonary Polymorphonuclear Leukocyte Killing, but Not Recruitment or PhagocytosisALCOHOLISM, Issue 9 2006Elizabeth A. Vander Top Background: People who smoke and abuse alcohol are uniquely susceptible to pulmonary infections caused by Streptococcus pneumoniae, the pneumococcus. The primary cellular defense against pneumococci within the lungs is the polymorphonuclear leukocyte (PMN). Cigarette smoke and ethanol (EtOH) are known to alter certain PMN functions, but little is known about their concurrent effects. Methods: Male Sprague,Dawley rats were exposed twice daily for 8 weeks to cigarette smoke (smoke-exposed) or room air (sham-exposed). During the final week of exposure, the rats were pair-fed a liquid diet containing either 36 or 0% EtOH calories. Polymorphonuclear leukocytes were prerecruited into the rats' lungs by transtracheal injection of lipopolysaccharide. Five hours later, the rats were infected transtracheally with S. pneumoniae, and PMN recruitment, phagocytosis, and bactericidal activity were quantified within their lungs. Chemokine levels were also measured in bronchoalveolar lavage fluids, lung homogenates, and sera. Results: Neither PMN recruitment nor phagocytic uptake of pneumococci was altered by EtOH ingestion or smoke exposure. Killing of the organisms, however, was significantly decreased in sham-exposed, but not smoke-exposed, rats ingesting EtOH. Parallel results were determined for serum cytokine-induced neutrophil chemoattractant-1 (CINC-1), with EtOH ingestion significantly decreasing the levels in sham-exposed, but not smoke-exposed, rats. Pulmonary levels of macrophage inflammatory protein-2 (MIP-2) and CINC-1 were highly elevated by the combination of EtOH and smoke. Conclusions: One week of EtOH ingestion by rats impaired the ability of their PMNs to kill S. pneumoniae within their lungs. This was not due to decreased recruitment of the PMNs to the lungs or to diminished phagocytosis of intrapulmonary pneumococci. The addition of twice-daily cigarette smoke exposure to this short-term EtOH ingestion model restored PMN bactericidal ability to levels observed in the absence of either treatment. These EtOH-induced and smoke-induced alterations in PMN killing may be related to alterations in both pulmonary and systemic inflammatory chemokine levels. [source] | ||||||||||