Biomedical subjects

S D Yan

Publications and source records attributed to S D Yan.

57 records · Page 4Linked to original sources

PubMedDate not supplied

Colony-stimulating factor in middle ear cholesteatoma.

Granulocyte-macrophage colony stimulating factor (GM-CSF) was found in human middle ear cholesteatoma tissues by immunohistochemical technique using mouse monoclonal anti-(human) GM-CSF IgG. Immunofluorescent staining showed the presence of GM-CSF in the peribasal area, in some suprabasal cells of the epithelium, and in the inflammatory connective tissue, especially in the monocytes and fibroblasts. These findings were confirmed by the immunoperoxidase method. Staining of the external ear canal epithelium, however, was significantly weaker than that of the cholesteatoma epithelium. The presence of GM-CSF in cholesteatoma appears to be a response to inflammation occurring in the middle ear cavity. Moreover, our in vitro study showed that GM-CSF induced the proliferation and protein synthesis of basal keratinocytes. This study suggests that GM-CSF is involved in the development and destructive effects of middle ear cholesteatoma.

Cell Differentiation↗

PubMedDate not supplied

The role of tumor necrosis factor-alpha in bone resorption of cholesteatoma.

Recent investigations have indicated that cytokines such as tumor necrosis factor-alpha (TNF-alpha) play a potential role in the bone resorption associated with inflammatory diseases. In this immunoperoxidase study, TNF-alpha was localized in mononuclear cells, macrophages, fibroblasts, osteoblasts, and osteoclasts adjacent to bone resorption areas in both human and experimental middle ear cholesteatomas. In vitro, TNF-alpha stimulated monocytes to form multinucleated cells that demonstrate tartrate-resistant acid phosphatase activity, a marker enzyme for osteoclasts. These multinucleated osteoclast-like cells induce resorption of devitalized bone. The extent of bone resorption was increased by the co-cultures of osteoblasts and osteoclasts in the presence of TNF-alpha, suggesting that cell to cell interaction plays a significant role in bone resorption. Moreover, TNF-alpha was capable of stimulating macrophages to produce acid phosphatase and collagenase, and osteoblasts to produce prostaglandin E2 and collagenase. These chemical mediators have been known to lead to bone resorption. Our findings suggest that TNF-alpha may play an important clinical role in the destructive process of cholesteatoma.

Acid Phosphatase↗

PubMedDate not supplied

Alzheimer neurofibrillary lesions: molecular nature and potential roles of different components.

Neurofibrillary lesions found in Alzheimer disease (AD) are known to react with antibodies raised against different molecules. At least 20 components have been detected in neurofibrillary tangles. These components can be roughly categorized into five groups, which include structural proteins, kinases and other cytosolic enzymes, stress-related molecules, amyloid and amyloid binding proteins, and others. Among them, an abnormal form of microtubule associated protein tau, PHF-tau, is a major component of Alzheimer NFT. Kinases associated with NFT, especially those belonging to the family of proline-directed Ser/Thr kinases, are considered to be important for PHF-tau hyperphosphorylation. A potentially significant kinase is a Cdc2-related kinase, which is associated tightly with paired helical filaments, has a molecular weight of 33kDa and is different from other known Cdc2-related kinases. The possibility that some of the NFT-associated elements may play an active role in the pathogenesis of Alzheimer's disease was supported by recent studies, in which advanced glycated products and markers of oxidant stress were located in NFT. In addition, PHF-tau was found to be glycated, and in vitro glycated tau was capable of inducing oxidant stress. Further characterization of different components of NFT by biochemical and other approaches will be important for understanding the mechanisms involved in the supramolecular aggregation of PHF within NFT.

Alzheimer Disease↗