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Articles by G Peng
Total Records ( 2 ) for G Peng
  M. P Rivera , F. C Detterbeck , M. A Socinski , D. T Moore , M. J Edelman , T. M Jahan , R. H Ansari , J. D Luketich , G Peng , M Monberg , C. K Obasaju and R. J. Gralla
  Background:

Several chemotherapy agents, including gemcitabine and paclitaxel, have been reported to cause interstitial pneumonitis. The incidence of pulmonary toxicity from the combination of gemcitabine and paclitaxel is reported to be approximately 5%. In this report, pulmonary function test (PFT) results were analyzed from two similar randomized phase 2 trials that tested platinum and nonplatinum regimens preoperatively in patients with stage I or II non-small cell lung cancer (NSCLC).

Methods:

The regimens included gemcitabine plus carboplatin, paclitaxel, or cisplatin. PFT and dyspnea scores were obtained at baseline and postchemotherapy, and were compared to one of several secondary end points, including ability to undergo surgical resection.

Results:

Baseline PFT scores varied with smoking status. Mean levels of diffusing capacity of the lung for carbon monoxide (Dlco) adjusted for hemoglobin declined 8% from pre- to postinduction (Wilcoxon signed rank test, p < 0.0001). Changes in FVC, FEV1, and total lung capacity were not statistically significant after chemotherapy. Although 27% of patients in the study had some reduction in PFT results, only 2 of the 85 eligible patients did not undergo surgery due to PFT reduction following chemotherapy. One patient in the study experienced a clinically significant respiratory toxicity (grade 3 dyspnea). Pulmonary toxicity was only statistically associated with male gender.

Conclusion:

In the preoperative setting, gemcitabine-based chemotherapy was well tolerated. The most commonly affected PFT parameter postchemotherapy was the Dlco. Although 15% of patients had a significant reduction in the Dlco postchemotherapy, it did not correlate with clinical symptoms or affect the ability to undergo surgical resection.

  W Lu , P Ran , D Zhang , G Peng , B Li , N Zhong and J. Wang
 

In pulmonary arterial smooth muscle cells (PASMCs), Ca2+ influx through store-operated Ca2+ channels thought to be composed of canonical transient receptor potential (TRPC) proteins is an important determinant of intracellular free calcium concentration ([Ca2+]i) and pulmonary vascular tone. Sildenafil, a type V phosphodiesterase inhibitor that increases cellular cGMP, is recently identified as a promising agent for treatment of pulmonary hypertension. We previously demonstrated that chronic hypoxia elevated basal [Ca2+]i in PASMCs due in large part to enhanced store-operated Ca2+ entry (SOCE); moreover, ex vivo exposure to prolonged hypoxia (4% O2 for 60 h) upregulated TRPC1 and TRPC6 expression in PASMCs. We examined the effect of sildenafil on basal [Ca2+]i, SOCE, and the expression of TRPC in PASMCs under prolonged hypoxia exposure. We also examined the effect of sildenafil on TRPC1 and TRPC6 expression in pulmonary arterial smooth muscle (PA) from rats that developed chronically hypoxic pulmonary hypertension (CHPH). Compared with vehicle control, treatment with sildenafil (300 nM) inhibited prolonged hypoxia induced increases of 1) basal [Ca2+]i, 2) SOCE, and 3) mRNA and protein expression of TRPC in PASMCs. Moreover, sildenafil (50 mg · kg–1 · day–1) inhibited mRNA and protein expression of TRPC1 and TRPC6 in PA from chronically hypoxic (10% O2 for 21 days) rats, which was associated with decreased right ventricular pressure and right ventricular hypertrophy. Furthermore, we found, in PASMCs exposed to prolonged hypoxia, that knockdown of TRPC1 or TRPC6 by their specific small interference RNA attenuated the hypoxic increases of SOCE and basal [Ca2+]i, suggesting a cause and effect link between increases of TRPC1 and TRPC6 expression and the hypoxic increases of SOCE and basal [Ca2+]i. These results suggest that sildenafil may alter basal [Ca2+]i in PASMCs by decreasing SOCE through downregulation of TRPC1 and TRPC6 expression, thereby contributing to decreased vascular tone of pulmonary arteries during the development of CHPH.

 
 
 
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