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Articles by G Niu
Total Records ( 2 ) for G Niu
  Z Liu , M Liu , G Niu , Y Cheng and J. Fei

Transcriptional repression is as important as transcriptional activation in establishing cell-type specific patterns of gene expression. RE1-silencing transcription factor (REST), also known as neuronal restrictive silencing factor (NRSF), is a transcriptional regulator that represses a battery of neuronal differentiation genes in non-neuronal cells or in neural progenitor cells by binding to a specific DNA sequence (repressor element-1/neuron-restrictive silencer element, RE1/NRSE). REST/NRSF functions in the neuronal development are widely studied, however, little is known about target genes in various non-neuronal lineages that may result in cell differentiation. Here, we use RNA interference (RNAi) technology combined with the microarray strategy to identify potential REST/NRSF targets and RE1/NRSEs in human non-neuronal cell line HEK 293. Expression of 54 genes was up-regulated by inhibition of REST/NRSF in the HEK 293 cells according to the microarray experiment and 13 of those were further confirmed by quantitative RT-PCR. Our results confirmed the good confidence and reliability of current research data based on in silico, chromatin immunoprecipitation in combination with microarrays (ChIP-chip), and high-throughput sequencing (ChIP-seq). However, in view of the fact that thousands of genes have been testified or predicted to be recognized by REST/NRSF, our data show that only a few genes among those are directly up-regulated by the interaction of REST/NRSF with RE1/NRSEs sites in gene sequences.

  G Niu , B. J Scherlag , Z Lu , M Ghias , Y Zhang , E Patterson , T. W Dasari , S Zacharias , R Lazzara , W. M Jackman and S. S. Po

Background— The objective of this study was to develop an acute experimental model showing both focal and macroreentrant sustained atrial fibrillation (AF).

Methods and Results— In 31 anesthetized dogs, bilateral thoracotomies allowed the attachment of electrode catheters at the right and left superior pulmonary veins, atrial free walls, and atrial appendages. Acetylcholine, 100 mmol/L, was applied topically to either appendage. Sequential radiofrequency ablation was achieved for the ganglionated plexi (GP), found adjacent to the 4 pulmonary veins. In 12 separate studies, a propafenone bolus, 2 mg/kg, was given before and after GP ablations at the start of acetylcholine-induced AF.

Acetylcholine caused abrupt onset of AF (n=22) or induced AF by burst pacing (n=9) that lasted ≥10 minutes. Rapid, regular, or fractionated atrial electrograms were consistently seen (average cycle length, 37±7 ms) at the appendages versus cycle lengths of 114±23 ms at other atrial sites. After ablations of GP, AF abruptly terminated (n=25). In 6 dogs, sustained atrial tachyarrhythmias continued. Pacing at specific atrial sites organized electrograms of one atrium or also captured the other atrium. The latter resulted in termination when pacing was stopped in 4 of these 6 experiments. Propafenone did not change the duration of focal AF before GP ablation (17±9 versus 14±8 minutes; control, P=0.6) but terminated reentrant atrial tachyarrhythmias (12±3 versus 2±1 minutes, P=0.0009).

Conclusions— Before GP ablation, acetylcholine (100 mmol/L) induced sustained AF characterized by rapid, focal firing. GP ablations were associated with loss of focal firing and regularization of electrograms in both atria before termination. Propafenone failed to terminate focal AF but rapidly terminated entrainable macroreentrant atrial tachyarrhythmias.

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