scholarly journals Glial fibrillary acidic protein is localized in the lens epithelium.

1984 ◽  
Vol 98 (5) ◽  
pp. 1895-1898 ◽  
Author(s):  
J S Hatfield ◽  
R P Skoff ◽  
H Maisel ◽  
L Eng
Keyword(s):  
Glial Fibrillary Acidic Protein ◽  
Lens Epithelium ◽  
Acidic Protein ◽  
Similar Protein ◽  
Neural Origin ◽  
Mouse Lens

The epithelium of the mouse lens stains intensely with antisera to glial fibrillary acidic protein (GFAP). A protein co-migrating with GFAP and immunoreactive with antisera to GFAP can be demonstrated in lens epithelium protein extracts by immunoblots. GFAP has previously been considered unique to cells of neural origin, but this study demonstrates that ectodermally derived cells express GFAP or a highly similar protein.

The lens epithelium contains glial fibrillary acidic protein (GFAP)

1985 ◽  
Vol 8 ◽  
pp. 347-357 ◽  
Author(s):  
James S. Hatfield ◽  
Robert P. Skoff ◽  
Harry Maisel ◽  
Lawrence Eng ◽  
Darell D. Bigner
Keyword(s):  
Glial Fibrillary Acidic Protein ◽  
Lens Epithelium ◽  
Acidic Protein

Expression of glial fibrillary acidic protein, actin, fibronectin and factor VIII antigen in human astrocytomas

Pathology ◽  
1983 ◽  
Vol 15 (4) ◽  
pp. 373-378 ◽  
Author(s):  
Stephen J. Lolait ◽  
J.H. Harmer ◽  
G. Auteri ◽  
J.S. Pedersen ◽  
B.H. Toh
Keyword(s):  
Glial Fibrillary Acidic Protein ◽  
Factor Viii ◽  
Acidic Protein ◽  
Factor Viii Antigen ◽  
Human Astrocytomas

scholarly journals Changes in Plasma Glial Fibrillary Acidic Protein in Children Receiving Sevoflurane Anesthesia: A Preliminary Randomized Trial

2021 ◽  
Vol 10 (4) ◽  
pp. 662
Author(s):  
Eun-Hee Kim ◽  
Young-Eun Jang ◽  
Sang-Hwan Ji ◽  
Ji-Hyun Lee ◽  
Sung-Ae Cho ◽  
...  
Keyword(s):  
Glial Fibrillary Acidic Protein ◽  
Randomized Trial ◽  
Protein Concentration ◽  
Pediatric Patients ◽  
Neuronal Injury ◽  
Acidic Protein ◽  
Anesthesia Induction ◽  
Sevoflurane Anesthesia ◽  
Control Groups ◽  
Over Time

We investigated changes in plasma glial fibrillary acidic protein concentration during sevoflurane anesthesia induction in children < 3 years old and determined the effect of co-administering dexmedetomidine. This preliminary randomized trial included 60 pediatric patients who received sevoflurane anesthesia for >3 h. Patients were assigned to dexmedetomidine or control groups at a 1:1 ratio. The primary outcome was changes in plasma glial fibrillary acidic protein concentration of dexmedetomidine and control groups over time. Fifty-five patients were included in the final analysis. The median (interquartile range (IQR)) of the plasma glial fibrillary acidic protein level was 387.7 (298.9–510.8) pg·mL−1 immediately after anesthetic induction, 302.6 (250.9–412.5) pg·mL−1 at 30 min, and 321.9 (233.8–576.2) pg·mL−1 at 180 min after the first sample. These values did not change over time (p = 0.759). However, plasma glial fibrillary acidic protein increased after 180 min of infusion of dexmedetomidine compared with values at 30 min infusion (p = 0.04, mean difference and 95% confidence interval of 221.6 and 2.2 to 441.0 pg·mL−1). In conclusion, three hours of sevoflurane anesthesia in pediatric patients < 3 years old did not provoke neuronal injury assessed by the plasma biomarker. Further studies regarding the effect of prolonged dexmedetomidine infusion on anesthetic neuronal injury are required.

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