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Diagnostic Hallmark (diagnostic + hallmark)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Pathophysiology and therapy of pruritus in allergic and atopic diseases

ALLERGY, Issue 7 2010
J. Buddenkotte
To cite this article: Buddenkotte J, Steinhoff M. Pathophysiology and therapy of pruritus in allergic and atopic diseases. Allergy 2010; 65: 805,821. Abstract Pruritus (itch) is a major characteristic and one of the most debiliating symptoms in allergic and atopic diseases and the diagnostic hallmark of atopic dermatitis. Pruritus is regularly defined as an unpleasant sensation provoking the desire to scratch. Although we achieved rather good knowledge about certain inducers of itch such as neuropeptides, amines, ,-opioids, cytokines and proteases, for example, less is known about the pathophysiological specifities among the different diseases, and the therapeutic consequences which may derive thereoff. This review dissects the role of mediators, receptors and itch inhibitors on peripheral nerve endings, dorsal root ganglia, the spinal cord and the CNS leading to the amplification or , vice versa , suppression of pruritus. As the treatment of pruritus in allergic and atopic skin disease is still not satisfactory, knowing these pathways and mechanisms may lead to novel therapeutic approaches against this frequently encountered skin symptom. [source]

Neuromyelitis optica: Pathogenicity of patient immunoglobulin in vivo,

ANNALS OF NEUROLOGY, Issue 5 2009
Monika Bradl PhD
Objective Severe inflammation and astrocyte loss with profound demyelination in spinal cord and optic nerves are typical pathological features of neuromyelitis optica (NMO). A diagnostic hallmark of this disease is the presence of serum autoantibodies against the water channel aquaporin-4 (AQP-4) on astrocytes. Methods We induced acute T-cell,mediated experimental autoimmune encephalomyelitis in Lewis rats and confronted the animals with an additional application of immunoglobulins from AQP-4 antibody,positive and ,negative NMO patients, multiple sclerosis patients, and control subjects. Results The immunoglobulins from AQP-4 antibody,positive NMO patients are pathogenic. When they reach serum titers in experimental animals comparable with those seen in NMO patients, they augment clinical disease and induce lesions in the central nervous system that are similar in structure and distribution to those seen in NMO patients, consisting of AQP-4 and astrocyte loss, granulocytic infiltrates, T cells and activated macrophages/microglia cells, and an extensive immunoglobulin and complement deposition on astrocyte processes of the perivascular and superficial glia limitans. AQP-4 antibody containing NMO immunoglobulin injected into naïve rats, young rats with leaky blood,brain barrier, or after transfer of a nonencephalitogenic T-cell line did not induce disease or neuropathological alterations in the central nervous system. Absorption of NMO immunoglobulins with AQP-4,transfected cells, but not with mock-transfected control cells, reduced the AQP-4 antibody titers and was associated with a reduction of astrocyte pathology after transfer. Interpretation Human anti,AQP-4 antibodies are not only important in the diagnosis of NMO but also augment disease and induce NMO-like lesions in animals with T-cell,mediated brain inflammation. Ann Neurol 2009;66:630,643 [source]

Damage control , a possible non-proteolytic role for ubiquitin in limiting neurodegeneration

NEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 2 2001
D. A. Gray
Ubiquitin can be detected in the neuronal and glial inclusions that are the diagnostic hallmarks of a number of human neurodegenerative diseases. It has been assumed that the presence of ubiquitin signifies the failed attempt of the cell to remove abnormal protein structures, which have been allowed to aggregate. The burden of abnormal protein arising from genetic mutations or cumulative oxidative damage might in the course of time overwhelm the ubiquitin-proteasome pathway (whose responsibility it is to eliminate misfolded or damaged proteins). However, ubiquitin may still serve a protective purpose distinct from its role in proteolysis. The physical properties of ubiquitin are such that a surface coating of ubiquitin should preclude further growth of the aggregate, prevent non-productive interactions, and conceal the contents from detection mechanisms that might ultimately kill the cell. This ,nonstick coating' hypothesis makes predictions about the nature of the conjugated ubiquitin and the consequences of removing it. [source]

Large cell calcifying Sertoli cell tumor of the testis: Comparative immunohistochemical study with Leydig cell tumor

PATHOLOGY INTERNATIONAL, Issue 6 2005
Katsuaki Sato
Large cell calcifying Sertoli cell tumor is a rare type of testicular, tumor., Reported, herein, is, a, Japanese, patient with this tumor not associated with Carney's complex. An 11-year-old boy was admitted to hospital because of left testicular enlargement, and radical orchiectomy was performed. Macroscopically, the tumor was well circumscribed and had a maximum diameter of approximately 2 cm. The cut surface showed a yellow-white solid mass. Histologically, the tumor was composed of large neoplastic cells with abundant eosinophilic cytoplasm with a tubular, trabecular, and solid arrangement and loose myxoid stroma with irregularly shaped calcification. Immunohistochemically, the tumor cells were positive for vimentin, S-100 protein, calretinin, inhibin-,, melan-A, and CD10, and type IV collagen and laminin were observed in the extracellular matrix around the tumor cells. The distributions of melan-A, CD10, and mitochondria were characteristically patchy; in contrast, they were diffusely distributed in the cytoplasm in a control case of Leydig cell tumor. The differences in immunostaining patterns for melan-A, CD10, and mitochondria as well as positivity for S-100 protein-, might be useful diagnostic hallmarks of large cell calcifying Sertoli cell tumor for discrimination from Leydig cell tumor. [source]