Chromosomal aberrations and molecular weight of single-stranded DNA fragments in embryonic fibroblasts of 101/H and CBA mice

1981 ◽  
Vol 92 (3) ◽  
pp. 1231-1233
Author(s):  
T. G. Sjakste ◽  
I. G. Lilp ◽  
N. I. Sjakste
Keyword(s):  
Molecular Weight ◽  
Chromosomal Aberrations ◽  
Dna Fragments ◽  
Embryonic Fibroblasts ◽  
Single Stranded Dna ◽  
Cba Mice

scholarly journals Effects of Target Sequence and Sense versus Anti-sense Strands on Gene Correction with Single-stranded DNA Fragments

2008 ◽  
Vol 144 (4) ◽  
pp. 431-436 ◽  
Author(s):  
H. Kamiya ◽  
M. Uchiyama ◽  
Y. Nakatsu ◽  
T. Tsuzuki ◽  
H. Harashima
Keyword(s):  
Target Sequence ◽  
Dna Fragments ◽  
Gene Correction ◽  
Single Stranded Dna

High molecular weight DNA fragments are processed by caspase sensitive or caspase independent pathways in cultures of cerebellar granule neurons

2003 ◽  
Vol 984 (1-2) ◽  
pp. 111-121 ◽  
Author(s):  
Hege Holte Slagsvold ◽  
Carola Maria Rosseland ◽  
Chris Jacobs ◽  
Erica Khuong ◽  
Nina Kristoffersen ◽  
...  
Keyword(s):  
Molecular Weight ◽  
High Molecular Weight ◽  
Cerebellar Granule Neurons ◽  
Granule Neurons ◽  
Dna Fragments ◽  
High Molecular Weight Dna ◽  
Cerebellar Granule

Separation of single-stranded DNA fragments at a 10-nucleotide resolution by stretching in microfluidic channels

Lab on a Chip ◽  
2011 ◽  
Vol 11 (23) ◽  
pp. 4036 ◽  
Author(s):  
Jiamin Wu ◽  
Shuang-Liang Zhao ◽  
Lizeng Gao ◽  
Jianzhong Wu ◽  
Di Gao
Keyword(s):  
Microfluidic Channels ◽  
Dna Fragments ◽  
Single Stranded Dna ◽  
Nucleotide Resolution

scholarly journals Hyperglycemia Enhances DNA Fragmentation after Transient Cerebral Ischemia

2001 ◽  
Vol 21 (5) ◽  
pp. 568-576 ◽  
Author(s):  
Ping-An Li ◽  
Ingrid Rasquinha ◽  
Qing Ping He ◽  
Bo K. Siesjö ◽  
Katalin Csiszár ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Cell Death ◽  
Cytochrome C ◽  
Dna Fragmentation ◽  
Caspase 3 ◽  
Cingulate Cortex ◽  
Tunel Staining ◽  
Dna Fragments ◽  
Cytochrome C Release ◽  
Klenow Polymerase

Previous histopathologic results have suggested that one mechanism whereby hyperglycemia (HG) leads to exaggerated ischemic damage involves fragmentation of DNA. DNA fragmentation in normoglycemia (NG) and HG rats subjected to 30 minutes of forebrain ischemia was studied by terminal deoxynucleotidyl transferase mediated DNA nick-labeling (TUNEL) staining, by pulse-field gel electrophoresis (PFGE), and by ligation-mediated polymerase chain reaction (LM-PCR). High molecular weight DNA fragments were detected by PFGE, whereas low molecular weight DNA fragments were detected using LM-PCR techniques. The LM-PCR procedure was performed on DNA from test samples with blunt (without Klenow polymerase) and 3′-recessed ends (with Klenow polymerase). In addition, cytochrome c release and caspase-3 activation were studied by immunocytochemistry. Results show that HG causes cytochrome c release, activates caspase-3, and exacerbates DNA fragments induced by ischemia. Thus, in HG rats, but not in control or NGs, TUNEL-stained cells were found in the cingulate cortex, neocortex, thalamus, and dorsolateral crest of the striatum, where neuronal death was observed by conventional histopathology, and where both cytosolic cytochrome c and active caspase-3 were detected by confocal microscopy. In the neocortex, both blunt-ended and stagger-ended fragments were detected in HG, but not in NG rats. Electron microscopy (EM) analysis was performed in the cingulate cortex, where numerous TUNEL-positive neurons were observed. Although DNA fragmentation was detected by TUNEL staining and electrophoresis techniques, EM analysis failed to indicate apoptotic cell death. It is concluded that HG triggers a cell death pathway and exacerbates DNA fragmentation induced by ischemia.

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