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Articles by S Sheth
Total Records ( 2 ) for S Sheth
  M. B Parodi , P Iacono , A Papayannis , S Sheth and F. Bandello

Objective  To compare the effects on visual acuity of laser treatment (LT), photodynamic therapy (PDT) with verteporfin, and intravitreal bevacizumab treatment in patients with juxtafoveal choroidal neovascularization secondary to pathologic myopia.

Methods  This prospective randomized clinical investigation enrolled 54 patients, who were divided into 3 groups receiving PDT, LT, or intravitreal bevacizumab treatment. The anti–vascular endothelial growth factor group received 1.25 mg of intravitreal bevacizumab at baseline; retreatment was performed if persistent intraretinal or subretinal fluid evaluated on optical coherence tomography or if choroidal neovascularization progression was detected on fluorescein angiography. The PDT group received treatment following the Verteporfin in Photodynamic Therapy Study Group guidelines. The LT group was submitted to direct LT and received PDT treatment if subfoveal recurrence or progression was detected on fluorescein angiography. A change in best-corrected visual acuity was the primary outcome.

Results  The mean best-corrected visual acuity in the PDT group decreased from 0.52 logMAR (SD, 0.24 logMAR) at baseline to 0.72 logMAR (SD, 0.25 logMAR) at the end of the study (P = .002). The LT group showed substantial stabilization from mean baseline visual acuity (mean, 0.45 logMAR [SD, 0.27 logMAR]) to the 24-month (mean, 0.56 logMAR [SD, 0.34 logMAR) examination values. The mean best-corrected visual acuity in the anti–vascular endothelial growth factor group increased from 0.6 logMAR (SD, 0.3 logMAR) at baseline to 0.42 logMAR (SD, 0.35 logMAR) at the end of the study (P = .006).

Conclusions  Overall, bevacizumab treatment offers the best functional results during a 2-year follow-up. In view of the small size of the sample in this study and the relatively low frequency of juxtafoveal choroidal neovascularization secondary to pathologic myopia, a multicentric clinical trial is necessary to validate our results.

Published online February 8, 2010 (doi:10.1001/archophthalmol.2009.408).

  S Jajoo , D Mukherjea , S Kumar , S Sheth , T Kaur , L. P Rybak and V. Ramkumar

Exposure of cells to adenosine receptor (AR) agonists leads to receptor uncoupling from G proteins and downregulation of the A1AR. The receptor levels on the cell surface generally recover on withdrawal of the agonist, because of either translocation of the sequestered A1AR back to plasma membrane or de novo synthesis of A1AR. To examine the mechanism(s) underlying A1AR downregulation and recovery, we treated ductus deferens tumor (DDT1 MF-2) cells with the agonist R-phenylisopropyladenosine (R-PIA) and showed a decrease in membrane A1AR levels by 24 h, which was associated with an unexpected 11-fold increase in A1AR mRNA. Acute exposure of these cells to R-PIA resulted in a rapid translocation of β-arrestin1 to the plasma membrane. Knockdown of β-arrestin1 by short interfering RNA (siRNA) blocked R-PIA-mediated downregulation of the A1AR, suppressed R-PIA-dependent ERK1/2 and activator protein-1 (AP-1) activity, and reduced the induction of A1AR mRNA. Withdrawal of the agonist after a 24-h exposure resulted in rapid recovery of plasma membrane A1AR. This was dependent on the de novo protein synthesis and on the activity of ERK1/2 but independent of β-arrestin1 and nuclear factor-B. Together, these data suggest that exposure to A1AR agonist stimulates ERK1/2 activity via β-arrestin1, which subserves receptor uncoupling and downregulation, in addition to the induction of A1AR expression. We propose that such a pathway ensures both the termination of the agonist signal and recovery by priming the cell for rapid de novo synthesis of A1AR once the drug is terminated.

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