Increased expression of adaptor protein p66Shc has been associated with progression of diabetic nephropathy. Afferent arteriolar dilation and glomerular hyperfiltration in diabetes are due to increased K channel availability and activity. Hyperglycemia was induced in Dahl salt-sensitive (SS) rats in a model of diabetes induced by streptozotocin (STZ). Renal injury was evaluated in SS rats and genetically modified SS rats either lacking p66Shc (p66Shc knockout [p66ShcKO]) or expressing p66Shc mutant (p66Shc-S36A). Afferent arteriolar diameter responses during STZ-induced hyperfiltration were determined by using the juxtamedullary nephron technique. Albuminuria and glomerular injury were mitigated in p66ShcKO and p66Shc-S36A rats with STZ-induced diabetes. SS rats with STZ-induced diabetes had significantly increased afferent arteriolar diameter, whereas p66ShcKO and p66Shc-S36A rats did not. SS rats with STZ-induced diabetes, but not p66ShcKO or p66Shc-S36A rats with STZ-induced diabetes, had an increased vasodilator response to the K channel activator pinacidil. Likewise, the K inhibitor glibenclamide resulted in a greater decrease in afferent arteriolar diameter in SS rats with STZ-induced diabetes than in STZ-treated SS p66ShcKO and p66Shc-S36A rats. Using patch-clamp electrophysiology, we demonstrated that p66ShcKO decreases K channel activity. These results indicate that inactivation of the adaptor protein p66Shc decreases afferent arteriolar K channel activity and decreases renal damage in diabetic SS rats.
Congenital hemangiomas are benign vascular tumors, categorized by their postnatal behavior as rapidly involuting, non‐involuting, or partially involuting. They are typically solitary, with a predilection for the head or limbs near a joint. We present two infants with small, multifocal congenital nonprogressive hemangiomas of the skin, one associated with hepatic and intracranial lesions, and another with an in utero intracranial hemorrhage and hydrocephalus. These cases further extend the differential diagnosis of congenital multifocal vascular lesions or “hemangiomatosis.”
Background
Full-thickness lower eyelid defects after Mohs micrographic surgery are frequently referred out to oculoplastic surgery for reconstruction. Reconstructive options include wedge closure with or without canthotomy/cantholysis and tarsoconjunctival sliding flaps. Defects >50% of the eyelid margin have traditionally required the two-stage Hughes flap, leaving the patient with monocular vision for 3-6 weeks until pedicle division.
Objective
To demonstrate single-stage periosteal flaps performed by dermatologic surgeons can result in safe, functional, and cosmetically acceptable repairs for large full thickness eyelid defects.
Materials and Methods
An institutional review board-approved retrospective study of repairs performed by two dermatologic surgeons between January 2017 and July 2021 at the University of Minnesota. Patient demographics, operative notes, and follow-up notes were reviewed. Defect and follow up photos were scored using a visual analogue scale to assess aesthetic results.
Results
Ten cases were included in the analysis. Six patients were male and the average age was 62 years old. 8/10 were basal cell carcinoma and 2/10 were melanoma. The mean defect was 9.5 cm2, with a range of 1 cm2 to 24 cm2. The median cosmetic score was 85.8 +/- 10.7. There were no serious complications reported.
Conclusion
Mohs micrographic surgeons can safely and successfully reconstruct large, full thickness eyelid defects by periosteal flap.
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