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Pathological Aspects (pathological + aspect)

Distribution by Scientific Domains
Medical Sciences60%
Life Sciences40%

Selected Abstracts

Osteopontin is produced by mast cells and affects IgE-mediated degranulation and migration of mast cells

EUROPEAN JOURNAL OF IMMUNOLOGY, Issue 2 2008
Akiko Nagasaka
Abstract Osteopontin (OPN), originally discovered in bone as an extracellular matrix protein, was identified in many cell types in the immune system, presumably being involved in many aspects of pathogenesis of inflammatory and immune diseases. Mast cells are also involved in such pathological aspects by secreting multiple mediators. However, it has not been determined whether mast cells produce OPN and whether it affects their function. To test this, we used murine fetal skin-derived cultured mast cells (FSMC) and bone marrow-derived cultured mast cells. We found that OPN was spontaneously produced by FSMC and inducible by ionomycin and Fc,RI aggregation in bone marrow-derived cultured mast cells. In the presence of mast cell growth factors, FSMC were similarly generated from both OPN-deficient (OPN,/,) and -sufficient (OPN+/+) mice without significant differences in yield, purity, granularity, and viability. Using OPN,/, FSMC, we found that recombinant OPN augmented IgE-mediated degranulation and induced FSMC chemotaxis. Both effects were mediated by OPN receptors (i.e. CD44 and integrin,,v). IgE-mediated passive cutaneous anaphylaxis was significantly reduced in OPN,/, mice compared with OPN+/+ mice, indicating physiological relevance of OPN. These results indicate that OPN is a mast cell mediator, enhances mast cell responses to antigen, and thus may influence mast cell-related pathological conditions. See accompanying commentary at http://dx.doi.org/10.1002/eji200738131 [source]

The mouse MPTP model: gene expression changes in dopaminergic neurons

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 1 2003
Kati Kühn
Abstract Parkinson's disease (PD) is a common neurodegenerative disorder, characterized by the progressive loss of dopaminergic neurons in the substantia nigra. Although valuable animal models have been developed, our knowledge of the aetiology and pathogenic factors implicated in PD is still insufficient to develop causal therapeutic strategies aimed at halting its progression. The neurotoxicity induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is one of the most valuable models for analysing pathological aspects of PD. In this paper we studied the gene expression patterns underlying the pathogenesis of MPTP-induced neurodegeneration. We treated young and old C57BL/6 mice with different schedules of MPTP to induce degenerative processes that vary in intensity and time-course. During the first week after intoxication we used nonradioactive in situ -hybridization to investigate the expression patterns of genes associated with (i) dopamine metabolism and signalling; (ii) familial forms of PD; (iii) protein folding and (iv) energy metabolism. MPTP injections induced different severities of neuronal injury depending on the age of the animals and the schedule of administration as well as a significant degeneration in the striatum. In situ hybridization showed that MPTP intoxication initiated a number of gene expression changes that (i) were restricted to the neurons of the substantia nigra pars compacta; (ii) were correlated in intensity and number of changes with the age of the animals and the severity of histopathological disturbances; (iii) displayed in each a significant down-regulation by the end of one week after the last MPTP injection, but (iv) varied within one MPTP regimen in expression levels during the observation period. The subacute injection of MPTP into one-year-old mice induced the most severe changes in gene expression. All genes investigated were affected. However, ,-synuclein was the only gene that was exclusively up-regulated in MPTP-treated animals displaying cell death. [source]

The non-inherited gastrointestinal polyposis syndromes

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 3 2002
E. M. Ward
The non-inherited gastrointestinal polyposis syndromes represent a group of rare disorders characterized by the presence of multiple, non-adenomatous polyps on the gastrointestinal mucosa occurring in unrelated patients. We present here a review of the clinical and histo- pathological aspects of the syndromes to include the Cronkhite,Canada syndrome, hyperplastic polyposis and lipomatous polyposis. While infrequently encoun- tered, these diseases can have devastating clinical effects that may be aggravated by delays in diagnosis and treatment. Prompt accurate diagnosis and treatment of these uncommon disorders depend on a sound working knowledge of the distinct clinical and pathological features described herein. [source]

A rat model of hypereosinophilic syndrome

PATHOLOGY INTERNATIONAL, Issue 2 2001
Kenji Sano
Hypereosinophilia-occurring rats without chemical and antigen treatment have been maintained in our laboratory. The rat, Matsumoto Eosinophilia Shinshu (mes), showed hypereosinophilia at the age of 9 weeks or older and developed eosinophil-related inflammatory lesions in many organs. These lesions included: aortitis, granulomatous lesion in the mesenteric lymph node, inflammatory fibroid polyp of the stomach and pulmonary vasculitis with septal infiltration. These lesions were involved with cellular infiltration of eosinophils and macrophages, and deposition of eosinophilic crystals which immunohistologically showed major basic protein and eosinophilic peroxidase derived from eosinophilic lysosomal constituents. Although the distribution of lesions in mes is a little different from that of hypereosinophilic syndrome (HES) in humans, in that endomyocardial fibrosis appears in HES while aortitis appears in mes, mes is probably comparable with HES. The present paper describes the pathological aspects of the lesions in mes and discusses the pathogenesis of tissue injury related to eosinophilic infiltration. [source]

Enthesopathies as occupational stress markers: Evidence from the upper limb

AMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY, Issue 2 2010
Sébastien Villotte
Abstract Enthesopathies,that is, "musculo-skeletal stress markers",are frequently used to reconstruct past lifestyles and activity patterns. Relatively little attention has been paid in physical anthropology to methodological gaps implicit in this approach: almost all methods previously employed neglect current medical insights into enthesopathies and the distinction between healthy and pathological aspects has been arbitrary. This study presents a new visual method of studying fibrocartilaginous enthesopathies of the upper limb (modified from Villotte: Bull Mém Soc Anthropol Paris n.s. 18 (2006) 65,85), and application of this method to 367 males who died between the 18th and 20th centuries, from four European identified skeletal collections: the Christ Church Spitalfields Collection, the identified skeletal collection of the anthropological museum of the University of Coimbra, and the Sassari and Bologna collections of the museum of Anthropology, University of Bologna. The analysis, using generalized estimating equations to model repeated binary outcome variables, has established a strong link between enthesopathies and physical activity: men with occupations involving heavy manual tasks have significantly (P -value < 0.001) more lesions of the upper limbs than nonmanual and light manual workers. Probability of the presence of an enthesopathy also increases with age and is higher for the right side compared with the left. Our study failed to distinguish significant differences between the collections when adjusted for the other effects. It appears that enthesopathies can be used to reconstruct past lifestyles of populations if physical anthropologists: 1) pay attention to the choice of entheses in their studies and 2) use appropriate methods. Am J Phys Anthropol, 2010. © 2009 Wiley-Liss, Inc. [source]