scholarly journals Influence of Ki-67 and proliferating cell nuclear antigen expression on the biological behavior of ameloblastomas

2018 ◽  
Vol 6 (2) ◽  
pp. 27
Author(s):  
Alberto Rodriguez-Archilla ◽  
CarmenM Barragan-Muñoz
Keyword(s):  
Proliferating Cell Nuclear Antigen ◽  
Antigen Expression ◽  
Biological Behavior ◽  
Nuclear Antigen ◽  
Ki 67 ◽  
Proliferating Cell

Comparison of immunostainings for proliferating cell nuclear antigen and Ki-67 in human extraocular lesions

1997 ◽  
Vol 235 (12) ◽  
pp. 767-772 ◽  
Author(s):  
Tatsuo Kodama ◽  
Katsue Kawamoto ◽  
Tatsuro Kono ◽  
Yuzo Shibuya ◽  
Tomoichi Setogawa
Keyword(s):  
Proliferating Cell Nuclear Antigen ◽  
Nuclear Antigen ◽  
Ki 67 ◽  
Proliferating Cell

The Impact of 5-Azacytidine on Placental Weight, Glycoprotein Pattern and Proliferating Cell Nuclear Antigen Expression in Rat Placenta

Placenta ◽  
2007 ◽  
Vol 28 (8-9) ◽  
pp. 803-811 ◽  
Author(s):  
L. Šerman ◽  
M. Vlahović ◽  
M. Šijan ◽  
F. Bulić-Jakuš ◽  
A. Šerman ◽  
...  
Keyword(s):  
Proliferating Cell Nuclear Antigen ◽  
Antigen Expression ◽  
Placental Weight ◽  
Nuclear Antigen ◽  
The Impact ◽  
Proliferating Cell

scholarly journals An evaluation of antioxidant effects on recovery from postischemic acute renal failure.

1994 ◽  
Vol 4 (8) ◽  
pp. 1588-1597
Author(s):  
R A Zager ◽  
S M Fuerstenberg ◽  
P H Baehr ◽  
D Myerson ◽  
B Torok-Storb
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Dna Fragmentation ◽  
Proliferating Cell Nuclear Antigen ◽  
Antigen Expression ◽  
Nuclear Antigen ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Tubular Necrosis ◽  
Proliferating Cell

Xanthine oxidase (XO) activity and hydroxyl radical (.OH) formation are widely proposed mediators of renal reperfusion injury, potentially altering the severity of, and recovery from, postischemic acute renal failure. The goal of this study was to ascertain whether combination XO inhibitor (oxypurinol) and .OH scavenger (Na benzoate) therapy, given at the time of renal ischemia, alters the extent of: (1) tubular necrosis and filtration failure; (2) DNA fragmentation/apoptosis (assessed in situ by terminal deoxynucleotidyl transferase reactivity); (3) early tubular regenerative responses (proliferating cell nuclear antigen expression; (3H)thymidine incorporation); and (4) the rate and/or degree of functional and morphologic repair. The effects of XO inhibition, .OH scavengers, and "catalytic" iron (FeSO4) on human proximal tubular cell proliferation in vitro were also assessed with a newly established cell line (HK-2). Male Sprague-Dawley rats were subjected to 35 min of bilateral renal arterial occlusion with or without oxypurinol/benzoate therapy. These agents did not alter the extent of tubular necrosis or filtration failure, proliferating cell nuclear antigen expression or thymidine incorporation, or the rate/extent of renal functional/morphologic repair. DNA fragmentation did not precede tubular necrosis, and it was unaffected by antioxidant therapy. By 5 days postischemia, both treatment groups demonstrated regenerating epithelial fronds that protruded into the lumina. These structures contained terminal deoxynucleotidyl transferase-reactive, but morphologically intact, cells, suggesting the presence of apoptosis. Oxypurinol and .OH scavengers (benzoate; dimethylthiourea) suppressed in vitro tubular cell proliferation; conversely, catalytic Fe had a growth-stimulatory effect. These results suggest that: (1) XO inhibition/.OH scavenger therapy has no discernible net effect on postischemic acute renal failure; (2) DNA fragmentation does not precede tubular necrosis, suggesting that it is not a primary mediator of ischemic cell death; and (3) antioxidants can be antiproliferative for human tubular cells, possibly mitigating their potential beneficial effects.

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