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Articles by S Sheng
Total Records ( 2 ) for S Sheng
  Z Fu , M Wang , M Gucek , J Zhang , J Wu , L Jiang , R. E Monticone , B Khazan , R Telljohann , J Mattison , S Sheng , R. N Cole , G Spinetti , G Pintus , L Liu , F. D Kolodgie , R Virmani , H Spurgeon , D. K Ingram , A. D Everett , E. G Lakatta and J. E. Van Eyk
 

Advancing age induces aortic wall thickening that results from the concerted effects of numerous signaling proteins, many of which have yet to be identified. To search for novel proteins associated with aortic wall thickening, we have performed a comprehensive quantitative proteomic study to analyze aortic proteins from young (8 months) and old (30 months) rats and identified 50 proteins that significantly change in abundance with aging. One novel protein, the milk fat globule protein epidermal growth factor 8 (MFG-E8), increases 2.3-fold in abundance in old aorta. Transcription and translation analysis demonstrated that aortic MFG-E8 mRNA and protein levels increase with aging in several mammalian species including humans. Dual immunolabeling shows that MFG-E8 colocalizes with both angiotensin II and monocyte chemoattractant protein (MCP)-1 within vascular smooth muscle cells (VSMCs) of the thickened aged aortic wall. Exposure of early passage VSMCs from young aorta to angiotensin II markedly increases MFG-E8 and enhances invasive capacity to levels observed in VSMCs from old rats. Treatment of VSMCs with MFG-E8 increases MCP-1 expression and VSMCs invasion that are inhibited by the MCP-1 receptor blocker vCCI. Silencing MFG-E8 RNA substantially reduces MFG-E8 expression and VSMCs invasion capacity. The data indicate that arterial MFG-E8 significantly increases with aging and is a pivotal relay element within the angiotensin II/MCP-1/VSMC invasion signaling cascade. Thus, targeting of MFG-E8 within this signaling axis pathway is a potential novel therapy for the prevention and treatment of the age-associated vascular diseases such as atherosclerosis.

  R. H Mehta , S Sheng , S. M O'Brien , F. L Grover , J. S Gammie , T. B Ferguson , E. D Peterson and on behalf of the Society of Thoracic Surgeons National Cardiac Surgery Database Investigators
 

Background— Reoperation for bleeding represents an important complication in patients undergoing coronary artery bypass surgery (CABG). Yet, few studies have characterized risk factors and patient outcomes of this event.

Methods and Results— We evaluated 528 686 CABG patients at >800 hospitals in the Society of Thoracic Surgeons National Cardiac Database (2004 to 2007). Clinical features and in-hospital outcomes were evaluated in patients with and without reoperation for bleeding after CABG. Logistic regression was used to identify predictors of risk of this event and to estimate weights for an additive risk score. A total of 12 652 CABG patients (2.4%) required reoperation for bleeding. These rates remained fairly stable over time (2.2%, 2.3%, 2.5%, and 2.4% from 2004 to 2007, respectively). Although overall operative mortality was 4.5-fold higher in patients requiring reoperation for bleeding versus those who did not (2.0% versus 9.1%), this mortality risk declined significantly over time (11.3%, 9.5%, 8.8%, and 8.2% from 2004 to 2007, respectively, P for trend=0.0006). Factors associated with higher risk for reoperation were identified by multivariable analysis (c statistic=0.60) and summarized into a simple bedside risk score. The risk-score performed well when tested in the validation set (Hosmer-Lemeshow P=0.16).

Conclusions— Reoperation for bleeding remains an important morbid event after CABG. Nonetheless, death in patients with this complication has decreased over time. Our risk tool should allow estimation of patients risk for reoperation for bleeding and promote preventive measures when feasible in this at-risk group.

 
 
 
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