Unique Variation of Barber's Disease: A Case Report.

Barber's disease is an occupational-related disease in which small hair fragments penetrate the dermis of the hand. Although there is limited literature related to the topic, barber's disease classically involves the interdigital space of hairdressers' hands. In this case report, we report an undescribed variation of the condition. The case involves a female hair stylist who presented to the office with numerous hair splinters under the nail plate of her dominant thumb. Subsequent evaluation revealed cystic destruction of the distal phalanx of the thumb. Despite preoperative suspicion for osteomyelitis, pathology revealed reactive bone fragments associated with surrounding tenosynovial tissue and no evidence of osteomyelitis. The proposed etiology of this finding is the inflammatory process related to a hair abscess that formed with a sinus originating in the lateral nail fold. The goal of the case report is to bring to light yet another variation of barber's disease.

Oxidative stress and light-evoked responses of the posterior segment in a mouse model of diabetic retinopathy.

PURPOSE: To test the hypothesis that in a mouse model of diabetic retinopathy, oxidative stress is linked with impaired light-evoked expansion of choroidal thickness and subretinal space (SRS). METHODS: We examined nondiabetic mice (wild-type, wt) with and without administration of manganese, nondiabetic mice deficient in rod phototransduction (transducin alpha knockout; GNAT1(-/-)), and diabetic mice (untreated or treated with the antioxidant α-lipoic acid [LPA]). Magnetic resonance imaging (MRI) was used to measure light-evoked increases in choroidal thickness and the apparent diffusion coefficient (ADC) at 88% to 100% depth into the retina (i.e., the SRS layer). RESULTS: Choroidal thickness values were similar (P > 0.05) between all untreated nondiabetic dark-adapted groups and increased significantly (P < 0.05) with light; this expansion was subnormal (P < 0.05) in both diabetic groups. Apparent diffusion coefficient values in the SRS layer robustly increased (P < 0.05) in a light duration-dependent manner, and this effect was independent of the presence of Mn(2+). The light-stimulated increase in ADC at the location of the SRS was absent in GNAT1(-/-) and diabetic mice (P > 0.05). In diabetic mice, the light-dependent increase in SRS ADC was significantly (P < 0.05) restored with LPA. CONCLUSIONS: Apparent diffusion coefficient MRI is a sensitive method for evaluating choroid thickness and its light-evoked expansion together with phototransduction-dependent changes in the SRS layer in mice in vivo. Because ADC MRI exploits an endogenous contrast mechanism, its translational potential is promising; it can also be performed in concert with manganese-enhanced MRI (MEMRI). Our data support a link between diabetes-related oxidative stress and rod, but not choroidal, pathophysiology.

Confirming a prediction of the calcium hypothesis of photoreceptor aging in mice.

Prior work in healthy rats supported a calcium hypothesis of photoreceptor aging, wherein progressive age-related declines in photopic vision are explainable by the extent of earlier escalating d-cis-diltiazem-insensitive increases in photoreceptor L-type calcium channel (LTCC) activity in vivo. Unlike rats, healthy mice have relatively stable photopic vision until after 18 months of age. We therefore hypothesized that photoreceptor LTCC activity in mice would not progressively increase until after 18 months. In 2-5, 10, 18, and 26 months male C57Bl/6J mice, photoreceptor LTCC activity and retinal thickness were evaluated in vivo (manganese-enhanced magnetic resonance imaging) with some groups also treated with d-cis-diltiazem; visual performance was evaluated (optokinetic tracking). Data were calibrated for cone-only responses using mice without rod transducin (GNAT1-/-). Photopic vision was stable until after 18 months without retinal thinning or progressive increases in retinal manganese uptake. We measured an uptake spike at 10 months. This spike, unlike that in the rat, was diltiazem sensitive in the dark and diltiazem insensitive in the light. Between dark and light, uptake in inner retina of older mice was unequal (unlike that in 2-5 months mice); outer retinal uptake was similar to that in 2-5 months mice. Stable murine photopic visual performance and nonescalating photoreceptor LTCC activity before 18 months of age were consistent with a prediction of the calcium hypothesis. Stark differences in the temporal evolution of mouse and rat photoreceptor LTCC activity suggest the need for personalized identification of the retinal mechanisms contributing to declines in photopic vision to ensure success of future treatment efforts.