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Diverse Causes (diverse + cause)
Selected AbstractsNeuropathic pain: symptoms, models, and mechanismsDRUG DEVELOPMENT RESEARCH, Issue 4 2006Simon Beggs Abstract Peripheral neuropathic pain is the most debilitating of all clinical pain syndromes and affects a large and growing number of people worldwide. There are diverse causes for peripheral neuropathic pain, which may be experienced after traumatic nerve injury or from diseases that affect peripheral nerves, such as diabetes, HIV/AIDS, and cancer, and it can also result from toxic chemicals, such as cancer chemotherapy agents. Despite these varying causes, it is clear that neuropathic pain is due to persistent pathological alterations resulting in hyperexcitability in the peripheral and central nervous systems, and it is the neuropathology that must be targeted for effective therapy of which there is none presently available. Mechanistically, neuropathic pain is distinct from acute pain and inflammatory pain, for which many effective therapies are known. In this review, we describe the relationships between clinical symptoms and experimental models of peripheral neuropathic pain, and we provide a framework for understanding the potential mechanisms that involve primary neuronal dysfunction as well as pathological changes in neuron-glial signaling. Drug Dev. Res. 67:289,301, 2006. © 2006 Wiley-Liss, Inc. [source] Does habitat use explain large scale species richness patterns of aquatic beetles in Europe?ECOGRAPHY, Issue 2 2003Ignacio Ribera Regularities in species richness are widely observed but controversy continues over its mechanistic explanation. Because richness patterns are usually a compound measure derived from taxonomically diverse species with different ecological requirements, these analyses may confound diverse causes of species numbers. Here we investigate species richness in the aquatic beetle fauna of Europe, separating major taxonomic groups and two major ecological types, species occurring in standing and running water bodies. We collated species distributions for 800+ species of water beetles in 15 regions across western Europe. Species number in any of these regions was related to three variables: total area size, geographic connectedness of the area, and latitude. Pooled species numbers were accurately predicted, but correlations were different for species associated with either running or standing water. The former were mostly correlated with latitude, while the latter were only correlated with the measure of connectedness or with area size. These differences were generally also observed in each of the four phylogenetically independent lineages of aquatic Coleoptera when analysed separately. We propose that effects of habitat, in this case possibly mediated by different long term persistence of running and standing water bodies, impose constraints at the population or local level which, if effective over larger temporal and spatial scales, determine global patterns of species richness. [source] Ethnically diverse causes of Walker-Warburg syndrome (WWS): FCMD mutations are a more common cause of WWS outside of the Middle East,HUMAN MUTATION, Issue 11 2008M. Chiara Manzini Abstract Walker-Warburg syndrome (WWS) is a genetically heterogeneous autosomal recessive disease characterized by congenital muscular dystrophy, cobblestone lissencephaly, and ocular malformations. Mutations in six genes involved in the glycosylation of á-dystroglycan (POMT1, POMT2, POMGNT1, FCMD, FKRP and LARGE) have been identified in WWS patients, but account for only a portion of WWS cases. To better understand the genetics of WWS and establish the frequency and distribution of mutations across WWS genes, we genotyped all known loci in a cohort of 43 WWS patients of varying geographical and ethnic origin. Surprisingly, we reached a molecular diagnosis for 40% of our patients and found mutations in POMT1, POMT2, FCMD and FKRP, many of which were novel alleles, but no mutations in POMGNT1 or LARGE. Notably, the FCMD gene was a more common cause of WWS than previously expected in the European/American subset of our cohort, including all Ashkenazi Jewish cases, who carried the same founder mutation. © 2008 Wiley-Liss, Inc. [source] Bone vascular supply in monitor lizards (Squamata: Varanidae): Influence of size, growth, and phylogenyJOURNAL OF MORPHOLOGY, Issue 5 2008Vivian de Buffrénil Abstract Bone vascular canals occur irregularly in tetrapods; however, the reason why a species has or lacks bone canals remains poorly understood. Basically, this feature could depend on phylogenetic history, or result from diverse causes, especially cortical accretion rate. The Varanidae, a monophyletic clade that includes species with impressive size differences but similar morphologies, is an excellent model for this question. Cortical vascularization was studied in 20 monitor species, on three bones (femur, fibula, and tibia) that differ in their shaft diameters, and in the absolute growth speed of their diaphyseal cortices. In all species smaller than 398 mm SVL (133,397 mm in sample), bone cortices lack vascular canals, whereas all larger species (460,1,170 mm in sample) display canals. The size 398,460 mm SVL is thus a threshold for the appearance of the canals. The distribution of vascular and avascular bone tissues among species does not precisely reflect phylogenetic relationships. When present, vascular canals always occur in the femur and tibia, but are less frequent, sparser, and thinner in the fibula. Vascular density increases linearly with specific size but decreases exponentially during individual growth. In most species, canal orientation varies between individuals and is diverse in a single section. No clear relationship exists between canal orientation and vascular density. These results suggest that: a) the occurrence and density of bone vascular canals are basically dependant on specific size, not phylogenetic relationships; b) vascular density reflects the absolute growth rates of bone cortices; c) the orientation of vascular canals is a variable feature independent of phylogeny or growth rate. J. Morphol., 2008. © 2007 Wiley-Liss, Inc. [source] | ||||||||||