Plaque Types (plaque + type)

Distribution by Scientific Domains


Selected Abstracts


Expression of p53 in lesions and unaffected skin of patients with plaque-type and guttate psoriasis: A quantitative comparative study

THE JOURNAL OF DERMATOLOGY, Issue 6 2007
Ayça Cordan YAZICI
ABSTRACT Psoriasis is a common inflammatory and hyperproliferative skin disease characterized by hyperproliferation of keratinocytes. The pathogenesis of psoriasis has yet to be determined. The control of cell growth is a delicately balanced process, regulated by external signals or the internal genetic program of an individual cell. In psoriasis, these processes are disturbed and some candidate genes like p53 are suspected of being involved in the pathogenesis of the disease. The p53 protein is essential for the regulation of cell proliferation. The study was performed on 32 patients with psoriasis (24 plaque type, eight guttate type). Biopsy specimens for immunohistochemical determination of p53 protein expression were collected from both the lesional and the nonlesional skin sites that were not exposed to sun in all of the patients (n = 32). Taking the ultraviolet (UV) exposure of the skin into consideration, a third skin sample was taken from each patient (n = 7) who had lesions on the sun-exposed areas. Immunohistochemical assessment of p53 expression in skin was determined as p53 protein expression per 1000 cells (keratinocytes). The statistical analysis revealed that the expressions of p53 per 1000 cells were higher in non-sun-exposed lesional skin than the non-sun-exposed nonlesional skin, also in plaque-type psoriasis than guttate-type psoriasis (P = 0.000, P = 0.046, P = 0.037, respectively). There was a positive correlation between the p53 expression in non-sun-exposed lesional skin versus expression in sun-exposed lesional skin (cubic centimeters = 0.811, P = 0.027). Our results show a stronger association of elevated p53 expression with chronic rather than acute inflammatory psoriasis. This may indicate a mechanistic difference between plaque-type and guttate psoriasis. Alternatively, this could reflect a chronological course as the disease transitions from an acute to a chronic phase. [source]


Association of carotid artery atheromatous plaque types with cerebral perfusion

ANZ JOURNAL OF SURGERY, Issue 11 2009
Dong Yan Gao
Abstract Background:, In an attempt to define the association of internal carotid artery atheromatous plaque morphology with potential cerebral ischaemia, we have investigated the relationship of different carotid plaque types with defects in cerebral perfusion. Methods:, In 130 patients requiring surgical correction of internal carotid artery stenoses greater than 70%, defects in cerebral perfusion due to both haemodynamic insufficiency and intracerebral vessel occlusion were identified using single photon emission computed tomography scans (SPECT). Carotid artery plaques in these patients were classified as homogeneous or heterogeneous based on preoperative Doppler Duplex Scanning and on the macroscopic characteristics of the plaques recorded by the surgeon during carotid endarterectomy, with sub-classification into potentially embolus-generating and non- embolus-generating plaques. In individual patients, plaque types were then correlated with the perfusion defects found in the SPECT scans. Results:, Of 130 patients, 112 (86%) had cerebral perfusion defects. In 56 asymptomatic patients in the study, 48 (85.7%) had perfusion defects as did 64 (86.5%) of 74 symptomatic patients. Cerebral infarcts were seen in 41 (31.5%). Occlusive infarcts (66%) were twice as frequent as haemodynamic insufficiency infarcts (34%). Eighteen patients with small cerebral infarcts on SPECT scanning gave no medical history of cerebral symptoms. Statistical analysis of the results revealed that there was no statistically identifiable association between carotid plaque type and the generation of cerebral symptoms or infarction. Conclusion:, This study found that internal carotid plaque morphology has no statistically significant association with perfusion defects, symptoms or cerebral infarction in patients with significant internal carotid artery stenosis. Also, it is suggested that haemodynamic cerebral infarction may be more common that previously believed (34% of infarcts identified in the study). Further, it is suggested that plaque morphology alone is not an indication for carotid endarterectomy. [source]


Dense-core and diffuse A, plaques in TgCRND8 mice studied with synchrotron FTIR microspectroscopy

BIOPOLYMERS, Issue 4 2007
Margaret Rak
Abstract Plaques composed of the A, peptide are the main pathological feature of Alzheimer's disease. Dense-core plaques are fibrillar deposits of A,, showing all the classical properties of amyloid including ,-sheet secondary structure, while diffuse plaques are amorphous deposits. We studied both plaque types, using synchrotron infrared (IR) microspectroscopy, a technique that allows the chemical composition and average protein secondary structure to be investigated in situ. We examined plaques in hippocampal, cortical and caudal tissue from 5- to 21-month-old TgCRND8 mice, a transgenic model expressing doubly mutant amyloid precursor protein, and displaying impaired hippocampal function and robust pathology from an early age. Spectral analysis confirmed that the congophilic plaque cores were composed of protein in a ,-sheet conformation. The amide I maximum of plaque cores was at 1623 cm,1, and unlike for in vitro A, fibrils, the high-frequency (1680,1690 cm,1) component attributed to antiparallel ,-sheet was not observed. A significant elevation in phospholipids was found around dense-core plaques in TgCRND8 mice ranging in age from 5 to 21 months. In contrast, diffuse plaques were not associated with IR detectable changes in protein secondary structure or relative concentrations of any other tissue components. © 2007 Wiley Periodicals, Inc. Biopolymers 87: 207,217, 2007. This article was originally published online as an accepted preprint. The "Published Online" date corresponds to the preprint version. You can request a copy of the preprint by emailing the Biopolymers editorial office at biopolymers@wiley.com [source]