| Description |
48 leaves ; 29 cm |
| Note |
Printout. |
| Thesis |
Thesis (M.S.)--Saint Joseph College, Connecticut, 2000. |
| Bibliography |
Includes bibliographical references (leaves 43-48). |
| Summary |
"There is increasing evidence that interactions between the immune system and the central nervous system (CNS) may lead to the initiation of acute and chronic inflammatory conditions that may contribute to the pathogenesis of many neurodegenerative diseases. One possible mechanism of CNS cell damage is overexpression of inflammatory cytokines by activated astrocytes, leading to apoptic death of these cells ... The results of this study underscore the immense complexity and exquisite regulation of the cytokine network. In the limited in vitro environment of the culture dish, using a cloned cell line, there was evidence suggestive of regulatory mechanisms such as receptor downregulation, modification of cell signaling pathways, apoptosis, and suppression of inflammatory response by anti-inflammatory cytokines. The results also validate the growing belief in the dynamic and multifunctional nature of astroglial cells." |
| Subject |
Apoptosis.
|
|
Cell death.
|
|
Cytokines.
|
| Added Title |
Induction of apoptosis in rat C6 glioma cells |
|
