PubMed · 10839679
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
S Ansari, F Akhdar, K Moutaery. 1999. Recognizing child disability.. https://doi.org/10.1097/00004356-199909000-00012
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
During normal aging there is a reduction in white matter volume in the cerebral hemispheres and structural abnormalities in myelin in some parts of the central nervous system, but whether nerve fibers are lost with age and whether the myelin changes are ubiquitous is not known. Studying the optic nerve, which is a circumscribed bundle of nerve fibers, offers an opportunity to gain further insight into the effects of normal aging on white matter. The present study examined the optic nerves from young (4-10 years) and old (27-33 years) rhesus monkeys using light and electron microscopy. These nerves had been perfused transcardially to obtain optimal preservation of the tissue. Varying degrees of degeneration were encountered in all the optic nerves from the old monkeys. The changes included myelin abnormalities, similar to those reported in other parts of the central nervous system; the presence of degenerating axons and their sheaths; changes in neuroglial cells; and thickening of the trabeculae of connective tissue in the nerve. The total number of nerve fibers was reduced from an average of 1.6 x 10(6) in the young optic nerves to as few as 4 x 10(5) in one old monkey, and with one exception in all of the old optic nerves the packing density of nerve fibers was less than in any of the young optic nerves. The degenerative changes were most marked in those optic nerves that contained the fewest nerve fibers.
Using a novel transgenic mouse model of spontaneous mammary carcinoma, we show here that the IL-12/pulse IL-2 combination can induce rapid and complete regression of well-established autochthonous tumor in a setting where the host immune system has been conditioned by the full dynamic process of neoplastic progression and tumorigenesis. Further, this regimen inhibits neovascularization of established mammary tumors, and does so in conjunction with potent local induction of genes encoding the IFN-gamma- and TNF-alpha-inducible antiangiogenic chemokines IFN-inducible protein 10 and monokine induced by IFN-gamma. In contrast to untreated juvenile C3(1)TAg mice in which histologically normal mammary epithelium predictably undergoes progressive hyperplasia, atypical changes, and ultimately transition to overt carcinoma, the current studies also demonstrate a unique preventative therapeutic role for IL-12/pulse IL-2. In juvenile mice, early administration of IL-12/pulse IL-2 markedly limits the expected genetically programmed neoplastic transition within the mammary epithelium and does so in conjunction with enhancement of constitutive Fas and pronounced induction of local Fas ligand gene expression, T cell infiltration, and induction of apoptosis within the mammary epithelium. These events occur in the absence of a durable Ag-specific memory response. Thus, this novel model system demonstrates that the potent therapeutic activity of the IL-12/pulse IL-2 combination rapidly engages potent apoptotic and antiangiogenic mechanisms that remain active during the delivery of IL-12/pulse IL-2. The results also demonstrate that these mechanisms are active against established tumor as well as developing preneoplastic lesions.
The choroid plexus in adult rats was examined for any structural alteration or apoptotic cell death following a high altitude exposure which leads to the development of hypobaric hypoxia due to reduced oxygen tension in the atmospheric air. Caspase-3 (a protease which mediates apoptosis) immunoreactivity was absent in the choroid plexus epithelial cells in the control rats and following altitude exposure; Bcl-2 (anti-apoptotic protein) and Bax (pro-apoptotic protein) immunoreactivity were upregulated at 3 h-2 days following the altitude exposure when compared to the controls but not in longer surviving rats. At the ultrastructural level, glycogen particles and vacuoles were observed in some epithelial cells at 7 days following the altitude exposure. It is suggested that transient exposure to high altitude may not cause much damage to the choroid plexus epithelial cells except for some structural alteration which may be due to altered metabolism of the cells in response to hypobaric hypoxia.