The high sensitivity of night vision requires that rod photoreceptors reliably and reproducibly signal the absorption of single photons, a process that depends on tight regulation of intracellular cGMP concentration through the phototransduction cascade. Here in the mouse (Mus musculus), we studied a single-site D167A mutation of the gene for the a subunit of rod photoreceptor phosphodiesterase (PDEA), made with the aim of removing a noncatalytic binding site for cGMP. This mutation unexpectedly eliminated nearly all PDEA expression and reduced expression of the b subunit (PDEB) to ;5%-10% of WT. The remaining PDE had nearly normal specific activity; degeneration was slow, with 50%-60% of rods remaining after 6 months. Responses were larger and more sensitive than normal but slower in rise and decay, probably from slower dark turnover of cGMP. Remarkably, responses became much less reproducible than WT, with response variance increasing for amplitude by over 10-fold, and for latency and time-to-peak by .100fold. We hypothesize that the increase in variance is the result of greater variability in the dark-resting concentration of cGMP, produced by spatial and temporal nonuniformity in spontaneous PDE activity. This variability decreased as stimuli were made brighter, presumably because of greater spatial uniformity of phototransduction and the approach to saturation. We conclude that the constancy of the rod response depends critically on PDE expression to maintain adequate spontaneous PDE activity, so that the concentration of second messenger is relatively uniform throughout the outer segment.
Introduction: Forearm fractures are a common pediatric injury. Currently, there is no consensus on treatment for fractures that recur following initial surgical fixation. The objective of this study was to investigate the subsequent fracture rate and patterns and describe the treatment of these forearm fractures. Methods: We retrospectively identified patients who underwent surgical treatment for an initial forearm fracture at our institution between 2011 and 2019. Patients were included if they sustained a diaphyseal or metadiaphyseal forearm fracture that was initially treated surgically with a plate and screw construct (plate) or elastic stable intramedullary nail (ESIN), and if they subsequently sustained another fracture that was treated at our institution. Results: A total of 349 forearm fractures were treated surgically with ESIN or a plate fixation. Of these, 24 sustained another fracture, yielding a subsequent fracture rate of 10.9% for the plate cohort and 5.1% for the ESIN cohort (P=0.056). The majority of plate refractures (90%) occurred at the proximal or distal plate edge, while 79% of the fractures treated previously with ESINs occurred at the initial fracture site (P<0.001). Ninety percent of plate refractures required revision surgery, with 50% underwent plate removal and conversion to ESIN, and 40% underwent revision plating. Within the ESIN cohort, 64% were treated nonsurgically, 21% underwent revision ESINs, and 14% underwent revision plating. Tourniquet time for revision surgeries were shorter for the ESIN cohort (46 vs. 92 min; P=0.012). In both cohorts, all revision surgeries had no complications and healed with evidence of radiographic union. However, 9 patients (37.5%) underwent implant removal (3 plates and 6 ESINs) after subsequent fracture healing. Conclusions: This is the first study to characterize subsequent forearm fractures following both ESIN and plate fixation and to describe and compare treatment options. Consistent with the literature, refractures following surgical fixation of pediatric forearm fractures may occur at a rate ranging from 5% to 11%. ESINs are both less invasive at the time of initial surgery and can often be treated nonoperatively if there is a subsequent fracture, while plate refractures are more likely to be treated with a second surgery and have a longer average surgery time. Level of Evidence: Level IV—retrospective case series.
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