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Articles by M. J Jiang
Total Records ( 3 ) for M. J Jiang
  Y Cheng , Z. q Li , J. z Huang , F Xue , M. j Jiang , K. m Wu and Q. p. Wang
 

Objectives  To apply the technique of injection of a combination of autologous fascia lata and fat into the vocal fold via the cricothyroid gap for unilateral vocal fold paralysis and to evaluate the therapeutic effect in 12 patients who underwent the procedure.

Design  Retrospective analysis of 12 patients.

Setting  Academic research.

Patients  A mixture of autologous fascia lata and fat was injected into the thyroarytenoid muscle of the paralyzed vocal fold in 12 patients.

Main Outcome Measures  Videolaryngostroboscopy was performed to observe the changes to the vocal fold. The patients' phonatory function before and after surgery was assessed by computerized acoustic analysis and by blinded perceptual evaluation.

Results  Videolaryngostroboscopy demonstrated that the paralyzed vocal folds in these patients were pushed medially after the procedure. Statistically significant improvements were found in the perturbation measurements (jitter and shimmer), harmonics to noise ratio, and maximum phonation time. Ratings by a panel of voice experts also showed each voice to be statistically significantly improved after the procedure. No complications were noted.

Conclusion  A combination of autologous fascia lata and fat injected into the vocal fold for unilateral vocal fold paralysis is a safe and effective therapy.

  Y. S Tsai , P. J Tsai , M. J Jiang , T. Y Chou , A Pendse , H. S Kim and N. Maeda
 

Mutations and polymorphisms in PPARG have been linked to adiposity and partial lipodystrophy in humans. However, how disturbances in PPARG lead to depot-specific effects on adipose tissue, as shown by the characteristic aberrant fat distribution in patients, remains unclear. By manipulating the 3'-untranslated region of the Pparg gene, we have generated mice with peroxisome proliferator-activated receptor (PPAR) gene expression ranging from 25% to 100% normal. Basal levels of PPAR transcripts between 50% and approximately 100% had no significant effect on body weight, fat mass, and insulin sensitivity. In contrast, mice with 25% normal PPAR expression exhibited reduced body weight and total fat mass, insulin resistance, and dyslipidemia. Interestingly, fat mass was selectively reduced in perigonadal depot without significant changes in inguinal and other depots. Expression of adipogenic factor CCAAT enhancer binding protein- and some other metabolic genes containing peroxisome proliferator response element were reduced in a perigonadal depot-specific fashion. This was further associated with depot-specific reduction in the expression of adipokines, increased expression of TNF, and increased ectopic lipid deposition in muscles. Together, these results underscore the differential sensitivity of the individual fat depots on PPAR availability as an underlying mechanism of partial lipodystrophy.

  Y. L Huang , C. M Wu , G. Y Shi , G. C. C Wu , H Lee , M. J Jiang , H. L Wu and H. Y. Yang
 

Nestin is an intermediate filament protein mainly expressed in muscle and neural progenitors. Recently, we reported that nestin is expressed in rat vascular smooth muscle cells (VSMCs), disappears after serum-deprivation and then is re-expressed again following EGF stimulation. As the function of nestin in VSMCs remains unknown, its anti-apoptotic function was investigated in this study. We first showed that cell viability of nestin-depleted cells following H2O2 treatments decreased by nestin RNAi. Further DNA laddering analysis and flow cytometry results demonstrated that this loss of cell viability was mediated through apoptosis. In addition, caspase-9, caspase-3 and PARP were activated in nestin-depleted VSMCs following H2O2 treatments, indicating that nestin has an upstream inhibitory effect on caspase activation. It is well known that EGF serves as a survival factor in rat VSMCs. Here, we show that the cytoprotective effect of EGF was prevented by nestin RNAi. In addition, the inhibition of Cdk5 prevented Bcl-2 phosphorylation and enhanced H2O2-induced caspase-3 activation as well as subsequent DNA fragmentation. Taken together, these results provide evidence for another cytoprotective role of EGF in that it is mediated through its stimulation of nestin expression which leads to the prevention of caspase activation by Cdk-5-induced Bcl-2 phosphorylation in rat VSMCs.

 
 
 
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