Biomedical subjects

L F Eng

Publications and source records attributed to L F Eng.

148 records · Page 9Linked to original sources

PubMedDate not supplied

Increase in glial fibrillary acidic protein following neural trauma.

Immunohistochemical staining and quantitative evaluation of glial fibrillary acidic protein (GFAP) were carried out in a stab wound model of neural trauma in the rat. Increased GFAP staining was detected in reactive cortical astrocytes in the vicinity of the wound at 3, 7, and 30 d following injury. Western blots immunostained for GFAP also demonstrated an increase in GFAP in homogenates from the lesioned cortex, compared to the contralateral control side, on days 3, 7, and 30. Specific activity of GFAP expressed as a ratio of lesion/control values showed a fivefold increase from day 0 to day 7, with no further change on day 30. We conclude that neural trauma elicits a quantitative increase in GFAP in the rat cortex during the first week following injury. This increase correlates with both astrocyte hyperthrophy and proliferation. Thus, specific activity of GFAP is a reliable indicator of the onset and progression of astrogliosis in neural trauma.

Animals↗

PubMedDate not supplied

Solitary retinal astrocytoma.

The clinicopathologic features of retinal or optic disc astrocytomas are discussed based on eighteen reported cases. In addition, a new case of solitary retinal astrocytoma in a patient without other stigmata of phakomatosis is described. The tumor was prominently vascular and caused total exudative retinal detachment. It doubled in diameter over the seven months prior to enucleation, which was dictated by the occurrence of neovascular glaucoma. The astrocytic nature of the lesion was confirmed by immunohistochemical techniques (glial fibrillary acidic protein stain) and by electron microscopy.

Adolescent↗

PubMedDate not supplied

[3H]thymidine labeling of astrocytes in experimental allergic encephalomyelitis.

In acute experimental allergic encephalomyelitis (EAE), astrocytes in spinal cord tissue hypertrophy and stain intensely with antibody to the glial fibrillary acidic protein (GFAP). We attempted to determine if this activation is a result solely of hypertrophy of existing astrocytes or if astrocyte division might also occur. Lewis rats in various stages of acute EAE were injected with [3H]thymidine, the spinal cord sections were prepared, immunostained for GFAP and processed for radioautography. In spinal cords from rats administered thymidine on days 11-15 after sensitization a large number of mononuclear cells showed radioactive label. Many of these labeled cells, most likely monocytes and lymphocytes, were associated with inflammatory lesions, but others were located in the CNS parenchyma at great distances from the lesions. Most cells staining for the GFAP were hypertrophied with greatly extended cell processes, and the nuclei of some of these cells identified as astrocytes were overlaid with silver grains, indicating uptake of [3H]thymidine. In addition a few ependymal cells appeared to be labeled. No GFAP-stained cells from the Freund's adjuvant controls contained radioactive label. Similar studies using SJL/J mice with chronic relapsing EAE yielded very few labeled inflammatory cells or astrocytes. This study indicates that division takes place in some astrocytes in acute EAE, but occurs much less frequently in chronic EAE. Probably most of the increase in GFAP-stained material is a result of hypertrophy of astrocytes rather than of massive cell division.

Acute Disease↗

PubMedDate not supplied

Bilirubin toxicity and differentiation of cultured astrocytes.

OBJECTIVE: To study the toxicity of bilirubin in primary cultures of newborn rat cerebral cortical astrocytes. STUDY DESIGN: Primary cultures of newborn rat astrocytes were incubated at bilirubin concentrations of 0, 1, 5, 10, 25, 50, 100, 200, and 2000 microM, at a bilirubin:albumin molar ratio of 1.7. Bilirubin toxicity was determined by changes in cellular morphology, trypan blue staining, and lactate dehydrogenase (LDH) release into the culture medium at various times of incubation. To determine if differentiation of astrocytes affects bilirubin toxicity, cultures were treated with dibutyryl cyclic adenosine monophosphate. RESULTS: All three indices of toxicity showed a bilirubin concentration dependence. LDH release in experimental cultures was significantly elevated (p < 0.05) above that of control cultures by 24 hours at bilirubin concentrations of > or = 100 microM. The absolute amount of LDH release differed significantly between the 200 and 2000 microM cultures from 1.5 to 24 hours, after which duration of exposure appeared to take over and all cultures approached maximum. LDH release for the lower concentrations all reached maximum by 120 hours, except for the 1 microM cultures, which showed no significant elevation above control throughout the study period. At 100 and 200 microM bilirubin, LDH release by untreated cells was significantly higher (p < 0.05) than release by treated cells by 36 hours. CONCLUSION: Undifferentiated astrocytes appeared to be more sensitive to bilirubin toxicity, which may correlate with the greater susceptibility of newborns to kernicteric injury. Studies with primary astrocyte culture may provide insight into how bilirubin sensitivity changes with brain development as well as the cellular and biochemical mechanisms of bilirubin encephalopathy.

Animals↗