Deep learning-based 3D OCT imaging for detection of lamina cribrosa defects in eyes with high myopia.

The lamina cribrosa (LC) is a collagenous tissue located in the optic nerve head, and its dissection is observed in eyes with pathologic myopia as a LC defect (LCD). The diagnosis of LCD has been difficult because the LC is located deep beneath the retinal nerve fibers. The purpose of this study was to determine the prevalence and three-dimensional shape of LCDs in highly myopic eyes. Swept-source OCT scan images of a 3 × 3-mm cube centered on the optic disc were obtained from 119 eyes of 62 highly myopic patients. Each LC was manually labelled in cross-sectional OCT images along the axial, coronal, and sagittal planes. A deep convolutional neural network (DCNN) was trained with the manually labeled images, and the trained DCNN was applied to the detection of the LC in every image in each plane. Three-dimensional images of the LC were generated from the labeled image of each eye. The results showed that LCDs were detected in 12 of the 42 (29%) eyes in which an LC was visible. The LCDs ran vertically at the temporal edge of the optic disc. In conclusion, 3D OCT imaging with the application of DCNN is helpful in diagnosing LCDs.

Prolonged but not short-duration blast waves elicit acute inflammation in a rodent model of primary blast limb trauma.

BACKGROUND: Blast injuries from conventional and improvised explosive devices account for 75% of injuries from current conflicts; over 70% of injuries involve the limbs. Variable duration and magnitude of blast wave loading occurs in real-life explosions and is hypothesised to cause different injuries. While a number of in vivo models report the inflammatory response to blast injuries, the extent of this response has not been investigated with respect to the duration of the primary blast wave. The relevance is that explosions in open air are of short duration compared to those in confined spaces. METHODS: Hindlimbs of adult Sprauge-Dawley rats were subjected to focal isolated primary blast waves of varying overpressure (1.8-3.65kPa) and duration (3.0-11.5ms), utilising a shock tube and purpose-built experimental rig. Rats were monitored during and after the blast. At 6 and 24h after exposure, blood, lungs, liver and muscle tissues were collected and prepared for histology and flow cytometry. RESULTS: At 6h, increases in circulating neutrophils and CD43Lo/His48Hi monocytes were observed in rats subjected to longer-duration blast waves. This was accompanied by increases in circulating pro-inflammatory chemo/cytokines KC and IL-6. No changes were observed with shorter-duration blast waves irrespective of overpressure. In all cases, no histological damage was observed in muscle, lung or liver. By 24h post-blast, all inflammatory parameters had normalised. CONCLUSIONS: We report the development of a rodent model of primary blast limb trauma that is the first to highlight an important role played by blast wave duration and magnitude in initiating acute inflammatory response following limb injury in the absence of limb fracture or penetrating trauma. The combined biological and mechanical method developed can be used to further understand the complex effects of blast waves in a range of different tissues and organs in vivo.