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Epidemiologic evidence implicates cyclooxygenase activity in the pathogenesis of Alzheimer's disease, in which amyloid plaques have been found to contain increased levels of dimers and higher multimers of the amyloid β peptide. The product of the oxygenation of arachidonic acid by the cyclooxygenases, prostaglandin H[sub 2] (PGH[sub 2]), rearranges non-enzymatically to several prostaglandins, including the highly reactive γ-keto aldehydes, levuglandins E[sub 2] and D[sub 2]. We demonstrate that PGH[sub 2] markedly accelerates the formation of dimers and higher oligomers of amyloid β[sub 1]-42- This is associated with the formation of levuglandin adducts of the peptide. These findings provide the molecular basis for a hypothesis linking cyclooxygenase activity to the formation of oligomers of amyloid β. [ABSTRACT FROM AUTHOR]

Numerous in vitro and cell culture experiments indicate that oxidative damage decreases astrocyte glutamate transport activity, and it has been proposed that products of lipid peroxidation, particularly 4-hydroxy-2-nonenal, may contribute to neurodegenerative diseases via inhibition of glutamate or glucose transporter activity. We have directly tested the hypothesis that lipid peroxidation products impair glutamate and glucose transport in vivo. Lipid peroxidation products that irreversibly modify protein lysyl residues caused a two- to sixfold elevation in extracellular glutamate in striatum and cerebral cortex of both freely moving and anesthetized rats undergoing microdialysis. No concomitant change in extracellular glucose concentrations was observed. Furthermore, lipid peroxidation product-evoked extracellular glutamate appeared to be derived from nonneuronal sources. Our results demonstrate a biochemical mechanism whereby oxidative damage products can increase extracellular glutamate levels in vivo, providing support for the proposal that oxidative damage leads to inhibition of glutamate transport and thereby may contribute to the progression of neurodegenerative diseases. [Copyright &y& Elsevier]

Liesagang-like rings (LR) are periodic structures with equally spaced radial striations formed by a process that involves diffusion, nucleation, flocculation or precipitation, and supersaturation. Being more common in vitro, on rare occasions also reported in vivo in association with inflammatory or cystic lesions and confused with parasites or calcification on needle aspirates. The current paper documents that LRs may be seen in noncystic and noninflammatory changes of the breast. [ABSTRACT FROM AUTHOR]

The article focuses on a study conducted by the authors on presence of cell polarity reversal in low-grade serous carcinomas (LGSCs) and micropapillary serous borderline tumours (M-SBTs) with application of immunohistochemical markers. Topics discussed include micropapillary growth patterns of LGSCs and M-SBTs, usage of epithelial cadherin (E-cadherin) for identifying cell polarity reversal and circumferential staining of boderline tumors.

Carbonyl stress from products of lipid peroxidation, such as 4-hydroxynonenal (HNE), and products of sugars in diabetes mellitus, such as methylglyoxal (MG) and glyoxal (G), may contribute to neurodegeneration in Alzheimer's disease (AD). We tested the hypothesis that these carbonyls alter the proposed central pathogenic mechanism of AD, intracellular amyloid-β (Aβ)-mediated cytotoxicity, using a human neuroblastoma cell line that conditionally expresses carboxy-terminal fragments (CTFs) of the amyloid precursor protein. HNE was a potent cytotoxin, whereas G was mildly cytotoxic; cytotoxicity from each was independent of Aβ/CTF expression and not altered by α-tocopherol. In contrast, MG cytotoxicity was enhanced by the induced expression of Aβ/CTFs and suppressed by α-tocopherol. α-tocopherol cytoprotection was accompanied by decreased Aβ/CTF aggregation. G also promoted β/CTF aggregation but by mechanisms unaffected byα-tocopherol treatment. Our findings showed that Aβ/CTF aggregation and cytotoxicity may be profoundly altered by aldehydes associated with diabetes and that in the case of MG, this process is suppressed by α-tocopherol. Moreover, our results suggest that while intracellular aggregation of Aβ/CTFs may be necessary for the development of toxicity attributable to their expression in this model, the presence of high-molecular weight aggregated Aβ/CTFs does not invariably lead to cytotoxicity. [ABSTRACT FROM AUTHOR]

A 73-year-old woman was found to have a 1.7 cm axillary mass, for which a core needle biopsy was performed. The specimen revealed fragmented squamous epithelium surrounded by lymphoid tissue consistent with a squamous inclusion cyst in a lymph node, but a metastatic squamous cell carcinoma could not be excluded. Within one month, the lesion enlarged to 5 cm and was excised. Touch preparation cytology during intraoperative consultation displayed numerous single and sheets of atypical epithelioid cells with enlarged nuclei and occasional mitoses, suggesting a carcinoma. However, multinucleated giant cells and neutrophils in the background indicated reactive changes. We interpreted the touch preparation as atypical and recommended conservative surgical management. Permanent sections revealed a ruptured squamous inclusion cyst in a lymph node with extensive reactive changes. Retrospectively, the atypical epithelioid cells on touch preparation corresponded to reactive histiocytes. This is the first case report of a rapidly enlarging ruptured squamous inclusion cyst in an axillary lymph node following core needle biopsy. Our case demonstrates the diagnostic challenges related to a ruptured squamous inclusion cyst and serves to inform the readers to consider this lesion in the differential diagnosis for similar situations. [ABSTRACT FROM AUTHOR]