Although intravitreal bevacizumab treatment is effective in inducing regression of ROP, the effect may be transient. Recurrence can occur later in the course than with conventional laser therapy. Late retinal detachment can occur despite early regression. Longterm favorable structural outcome may require extended observation and retreatment. Laser may be a useful treatment for recurrences.

Background and Purpose-Macrophage inflammatory protein (MIP)-1␣ is a well-characterized monocyte chemoattractant; its role in regulating monocyte and microglial recruitment and activation in the injured neonatal brain is unknown. We evaluated the impact of acute hypoxic-ischemic (HI) brain injury on the expression of MIP-1␣ in neonatal rat brain. Methods-To elicit forebrain ischemic injury, 7-day-old (P7) rats underwent right carotid ligation, followed by 2.5 hours of 8% oxygen exposure. We used an enzyme-linked immunosorbent assay and immunohistochemistry to detect MIP-1␣; double-labeling immunofluorescence assays were analyzed with confocal microscopy to identify cellular sources of MIP-1␣. Immunocytochemistry assays were also used to detect 2 MIP-1␣ receptors, CCR1 and CCR5. Results-We found marked increases in tissue concentrations of MIP-1␣ in the HI cerebral hemisphere, peaking from 8 to 72 hours after lesioning. Immunocytochemistry assays revealed that MIP-1␣ was constitutively expressed in physiologically activated microglia; from 8 to 120 hours after lesioning, MIP-1␣ immunoreactive monocytes and microglia accumulated in the lesion territory. In immunoreactive cells, MIP-1␣ was diffusely distributed throughout the cytoplasm at early post-HI time intervals; by 72 hours, MIP-1␣ immunoreactivity was typically concentrated adjacent to the nucleus, a pattern indicative of active MIP-1␣ production. In P7 to P12 brain, many cells expressed MIP-1␣ receptors; both CCR1 and CCR5 immunoreactivity were localized to endothelium and ependyma; CCR1-immunoreactive astrocytes and neurons and CCR5-immunoreactive microglia were also identified. Conclusions-These

The Focus NIGHT & DAY contact lens can improve subjective dry eye symptoms and visual acuity in patients with refractory dry eye disease secondary to GVHD.

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Recent experimental data indicate that inflammatory mediators contribute substantially to the pathogenesis of neonatal brain injury.1 Heightened interest in the pathogenetic role of inflammatory mediators in the immature nervous system stems from clinical observations linking detection of pro-inflammatory cytokines in the amniotic fluid and in the neonatal brain with adverse neurodevelopmental outcome.2,3 Studies in experimental models of hypoxic-ischemic and excitotoxic neonatal brain injury provide direct evidence for associated activation of proinflammatory mechanisms. -9The maturational stage of postnatal day (P)7 rat brain corresponds roughly with late-gestation human brain maturation. A well characterized model of acute excitotoxic brain injury, elicited by direct intracerebral (i.c.) administration of the glutamate agonist N-methyl-D-aspartate (NMDA) into P7 rat brain 10 facilitates analysis of the molecular and cellular responses elicited by NMDA receptor over-activation in vivo. In the rat, NMDA-induced brain injury is dose dependent and reproducible; susceptibility to NMDA-induced neurotoxicity peaks at P7.

Tumor necrosis factor (TNF)-alpha, a multifunctional pro-inflammatory cytokine, has been implicated in the pathogenesis of acute ischemic brain injury. Recent data also suggest that TNF-alpha is a clinically relevant mediator of neonatal brain injury. We hypothesized that inhibition of TNF-alpha activity would reduce excitotoxic brain injury in neonatal rats. To test this hypothesis, we evaluated the efficacy of a TNF binding protein (bp) in attenuating NMDA-induced injury in 7 day old rats. Intrastriatal co-injection of TNFbp (3.75 microg) with NMDA (10 nmol) reduced striatal injury by 26%; in contrast, intra-hippocampal co-injection of TNFbp (3.75 microg) with NMDA (10 nmol) increased hippocampal damage by 68%. These findings indicate that TNF-alpha may have both beneficial and deleterious effects in the injured neonatal brain.

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