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Articles by L. E. H. Smith
Total Records ( 2 ) for L. E. H. Smith
  C Wu , D. K VanderVeen , A Hellstrom , C Lofqvist and L. E. H. Smith
 

Objective  To validate longitudinal postnatal weight gain as a method for predicting severe retinopathy of prematurity (ROP) in a US cohort.

Methods  Both ROP evaluations and weekly weight measurements from birth to postmenstrual week 36 for 318 infants were entered into a computer-based surveillance system, WINROP. This system signaled an alarm when the rate of weight gain decreased compared with control subjects. Infants were classified into 3 groups: (1) no alarm, (2) low-risk alarm, or (3) high-risk alarm. Maximum ROP for each infant was categorized as (1) no ROP (immature or mature vascularization), (2) mild ROP (stage 1 or 2 ROP in zone II or III, without plus disease), or (3) severe ROP (any prethreshold, any stage 3, or threshold ROP). A high-risk alarm identified infants at risk for developing severe ROP.

Results  A high-risk alarm occurred in 81 infants (25.5%) and detected all infants who developed severe ROP a median of 9 weeks before diagnosis. The remaining infants received no alarm or a low-risk alarm. None of these infants developed more than mild ROP.

Conclusions  Longitudinal postnatal weight gain may help predict ROP. In a US cohort, the WINROP system had a sensitivity of 100% and identified infants early who developed severe ROP. With further validation, WINROP has the potential to safely reduce the number of ROP examinations.

  A Stahl , P Sapieha , K. M Connor , J. P SanGiovanni , J Chen , C. M Aderman , K. L Willett , N. M Krah , R. J Dennison , M. R Seaward , K. I Guerin , J Hua and L. E. H. Smith
  Rationale:

Omega3 long-chain polyunsaturated fatty acids (3-PUFAs) are powerful modulators of angiogenesis. However, little is known about the mechanisms governing 3-PUFA–dependent attenuation of angiogenesis.

Objective:

This study aims to identify a major mechanism by which 3-PUFAs attenuate retinal neovascularization.

Methods and Results:

Administering 3-PUFAs exclusively during the neovascular stage of the mouse model of oxygen-induced retinopathy induces a direct neovascularization reduction of more than 40% without altering vasoobliteration or the regrowth of normal vessels. Cotreatment with an inhibitor of peroxisome proliferator-activated receptor (PPAR) almost completely abrogates this effect. Inhibition of PPAR also reverses the 3-PUFA–induced reduction of retinal tumor necrosis factor-, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, endothelial selectin, and angiopoietin 2 but not vascular endothelial growth factor.

Conclusions:

These results identify a direct, PPAR-mediated effect of 3-PUFAs on retinal neovascularization formation and retinal angiogenic activation that is independent of vascular endothelial growth factor.

 
 
 
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