NPD1-mediated stereoselective regulation of BIRC3 expression through cREL is decisive for neural cell survival.

Neuroprotectin D1 (NPD1), a docosahexaenoic acid (DHA)-derived mediator, induces cell survival in uncompensated oxidative stress (OS), neurodegenerations or ischemic stroke. The molecular principles underlying this protection remain unresolved. We report here that, in retinal pigment epithelial cells, NPD1 induces nuclear translocation and cREL synthesis that, in turn, mediates BIRC3 transcription. NPD1 activates NF-κB by an alternate route to canonical signaling, so the opposing effects of TNFR1 and NPD1 on BIRC3 expression are not due to interaction/s between NF-κB pathways. RelB expression follows a similar pattern as BIRC3, indicating that NPD1 also is required to activate cREL-mediated RelB expression. These results suggest that cREL, which follows a periodic pattern augmented by the lipid mediator, regulates a cluster of NPD1-dependent genes after cREL nuclear translocation. BIRC3 silencing prevents NPD1 induction of survival against OS. Moreover, brain NPD1 biosynthesis and selective neuronal BIRC3 abundance are increased by DHA after experimental ischemic stroke followed by remarkable neurological recovery. Thus, NPD1 bioactivity governs key counter-regulatory gene transcription decisive for retinal and brain neural cell integrity when confronted with potential disruptions of homeostasis.

Palpebral myiasis.

Myiasis is most prevalent in Mexico, central and south America, tropical Africa, and the southwestern United States. Although dermal myiasis is rare in most of the United States, it is a disorder that may be seen in international travelers. In the United States, external myiasis is usually caused by the cattle botfly. We report here a case of ophthalmomyiasis involving the left upper eyelid of a child. We examined a six-year-old boy who presented to the Massachusetts Eye and Ear Infirmary (MEEI) in September 1998. He complained of persistent swelling of his left upper eyelid for the previous ten days. The edema and erythema were unresponsive to warm compresses and oral antibiotics. Ocular examination revealed a mild preseptal cellulitis of the left upper eyelid with a small draining fistula. On slit-lamp examination, we found one larva protruding intermittently from the fistula site. The larva was extracted with forceps, wrapped in a moist towel and sent in a jar to the parasitology laboratory. The specimen was identified as a Cuterebra larva by a parasitologist at the Harvard School of Public Health. One week later, the patient's eyelid edema and erythema had completely resolved.

Factors associated with the poor final visual outcome after traumatic hyphema.

In order to determine the factors related to the worse final visual outcome following nonperforating traumatic hyphema, the clinical characteristics of 18 patients with visual outcome of 0.1 or worse were compared with those of 166 patients with visual outcome of 0.15 or better. The presence of posterior segment injuries such as macula edema, retinal hemorrhage, epiretinal membrane, and choroidal rupture were significant factors of a poor final visual outcome (P < 0.01). The presence of anterior segment injuries such as corneal blood staining, traumatic mydriasis, iridodialysis, cataract, and lens subluxation had significant predictive factors on a poor final visual outcome and the concurrent posterior segment injuries were more frequent in these patients. Initial visual acuity of 0.1 or worse, glaucoma, vitreous hemorrhage, and eyelid laceration were also significant associations of a poor final visual outcome (P < 0.05). Patients with initially larger hyphema (grade I or more vs microscopic) and older age group (16 years or more vs 15 years or less) tended to have poor final visual acuities. Rebleeding was not associated with significant deterioration in visual prognosis. We conclude that the posterior segment injuries seem to be directly related to a poor visual outcome rather than the occurrence of secondary hemorrhage.