Kaempferol Protects Against Retinal Photoreceptor Degeneration in a Mouse Model of Light-Induced Retinal Injury.

Purpose: Age-related macular degeneration (AMD) is a leading cause of blindness in developed countries with little in the way of treatment that prevents progression to end-stage disease. Kaempferol (KF) is a plant-derived dietary flavonoid that has demonstrated as a strong antioxidant showing neuroprotection in stroke models. We hypothesize that KF has protective effects against retinal degeneration and may serve as a therapeutic agent against AMD. Methods: BALB/c albino mice were assigned to 1 of 2 groups: control-treated or KF-treated retinal light injury mice. Mice were exposed to 8,000 lux cool white fluorescent light for 2 h to induce light injury. Control or KF was injected intraperitoneally after light injury for 5 days. Scotopic electroretinography (ERG) was recorded before light injury and 7 days after light injury. The retinal morphology and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assays were performed after light injury. Results: ERG a- and b-wave amplitudes were significantly reduced in the retinal light injury group compared with the nonretinal light injury group. Retinal light injury produced markedly thinning of the outer nuclear layer along with significant TUNEL-positive signals. In contrast KF treatments significantly attenuated reduction of ERG a- and b- wave amplitudes and the loss of the outer nuclear layer. Conclusions: KF protects retinal photoreceptors and preserves retinal function against retinal degeneration caused by light injury. These initial findings suggest that KF may represent a novel therapy for retinal degenerative conditions such as AMD.

Protection of Retinal Function by Nucleoside Reverse Transcriptase Inhibitors Following Retinal Ischemia/Reperfusion Injury.

Purpose: Retinal ischemia/reperfusion (I/R) injury is a common cause of visual impairment and blindness for which there remain limited treatment options. Nucleoside reverse transcriptase inhibitors (NRTIs), such as zidovudine (AZT), have been shown to block the NLRP3 inflammasome and prevent retinal degeneration in a mouse model of age-related macular degeneration. The NLRP3 inflammasome has also been shown to be triggered in I/R injury. Therefore, we studied the neuroprotective effects of AZT using a pressure-induced retinal ischemia mouse model. Methods: C57BL/6J mice were randomly assigned to 1 of 2 treatment groups: vehicle-treated retinal I/R injury (n = 6) or AZT-treated retinal I/R injury (n = 6). Vehicle (1% dimethyl sulfoxide [DMSO] in phosphate-buffered saline [PBS]) or AZT 50 mg/kg in 1% DMSO in PBS were injected intraperitoneally twice daily for 5 days. On day 2 of treatment, retinal ischemia was induced by transient elevation of intraocular pressure for 45 min. Scotopic electroretinography (ERG) was used to quantify retinal function before and 1 week after retinal ischemic insult. Retinal morphology was examined 1 week after ischemic insult. Terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assays and caspase 1 immunostaining was performed 24 h after retinal I/R injury. Results: Following I/R injury, ERG a- and b-wave amplitudes were significantly reduced in the vehicle-treated mice. AZT treatment significantly attenuated I/R-induced loss of retinal function as compared with vehicle-treated mice. Additionally, AZT-treated mice experienced significantly less inner retinal thinning as compared with vehicle-treated mice. TUNEL-positive cells were prevalent in the vehicle-treated I/R injury mouse retinas compared with the AZT-treated I/R injury mouse retinas. More caspase-1 immunoreactivity was detected in ganglion cell layer and inner nuclear layer (INL) in vehicle-treated I/R injury group than in AZT-treated I/R injury group. Conclusion: AZT treatment resulted in relative preservation of retinal structure and function following ischemic insult as compared with controls. This suggests AZT may have therapeutic value in the management of retinal ischemic diseases.

Effects of corrective strabismus surgery on social anxiety and self-consciousness in adults.

PURPOSE: To report the results of a questionnaire-based interventional study to evaluate the effects of strabismus surgery on private self-consciousness, public self-consciousness, and social anxiety using a validated self-consciousness survey instrument. METHODS: Patients who underwent strabismus surgery completed a demographics and a self-consciousness scale form both pre- and postoperatively. The total and subscale (private self-consciousness, public self-consciousness, and social anxiety) summative scores were compared using the Wilcoxon signed-rank test, with statistically significant relationships defined as P < 0.05. Total and subscale summative scores were analyzed as such and by strabismus type, years of education, and marital status. RESULTS: Overall improvement was found postoperatively in total scores (P = 0.012), public self-consciousness scores (P = 0.009), and social anxiety scores (P = 0.028). Although improvement was noted for the private self-consciousness subscale (P = 0.188), it did not reach statistical significance. Subdivided according to strabismic and demographic subgroups, significant improvement was only noted in esotropic patients, college graduates, married/living partner/widowed patients, and separated/divorced patients. CONCLUSIONS: This study suggests that beyond functional and cosmetic improvements, strabismus surgery can result in improved public self-consciousness and social anxiety, with greatest effect noted in esotropic, college graduates, and nonsingle patients.

Protection of retinal function by sulforaphane following retinal ischemic injury.

Sulforaphane, a precursor of glucosinolate in cruciferous vegetables such as broccoli and cauliflower, has been shown to protect brain ischemic injury. In this study, we examined the effect of systemic administration of sulforaphane on retinal ischemic reperfusion injury. Intraocular pressure was elevated in two groups of C57BL/6 mice (n = 8 per group) for 45 min to induce retinal ischemic reperfusion injury. Following retinal ischemic reperfusion injury, vehicle (1% DMSO saline) or sulforaphane (25 mg/kg/day) was administered intraperitoneally daily for 5 days. Scotopic electroretinography (ERG) was used to quantify retinal function prior to and one-week after retinal ischemic insult. Retinal morphology was examined one week after ischemic insult. Following ischemic reperfusion injury, ERG a- and b-wave amplitudes were significantly reduced in the control mice. Sulforaphane treatment significantly attenuated ischemic-induced loss of retinal function as compared to vehicle treated mice. In vehicle treated mice, ischemic reperfusion injury produced marked thinning of the inner retinal layers, but the thinning of the inner retinal layers appeared significantly less with sulforaphane treatment. Thus, sulforaphane may be beneficial in the treatment of retinal disorders with ischemic reperfusion injury.

Amniotic band syndrome with significant orofacial clefts and disruptions and distortions of craniofacial structures.

Amniotic band syndrome (ABS) is a rare disorder in which bands of mesoderm that emanate from the chorionic side of the amnion and insert on the fetal body can generate a wide variety of disfiguring and disabling malformations. It usually is sporadic, and the incidence is approximately 1 in 15,000 live births, and affected children typically require involvement of several pediatric surgical subspecialties. The authors describe a case of ABS with extensive craniofacial anomalies.