Open Globe Injury Patient Identification in Warfare Clinical Notes.

The aim of this study is to utilize the Defense and Veterans Eye Injury and Vision Registry clinical data derived from DoD and VA medical systems which include documentation of care while in combat, and develop methods for comprehensive and reliable Open Globe Injury (OGI) patient identification. In particular, we focus on the use of free-form clinical notes, since structured data, such as diagnoses or procedure codes, as found in early post-trauma clinical records, may not be a comprehensive and reliable indicator of OGIs. The challenges of the task include low incidence rate (few positive examples), idiosyncratic military ophthalmology vocabulary, extreme brevity of notes, specialized abbreviations, typos and misspellings. We modeled the problem as a text classification task and utilized a combination of supervised learning (SVMs) and word embeddings learnt in a unsupervised manner, achieving a precision of 92.50% and a recall of89.83%o. The described techniques are applicable to patient cohort identification with limited training data and low incidence rate.

Effect of diabetic retinopathy and panretinal photocoagulation on retinal nerve fiber layer and optic nerve appearance.

OBJECTIVE: To determine if panretinal photocoagulation (PRP) alters retinal nerve fiber layer (RNFL) thickness and optic nerve appearance. METHODS: Patients with diabetes who did and did not undergo PRP and nondiabetic control subjects were enrolled in a prospective study. Participants underwent optical coherence tomography of the peripapillary retina and optic nerve. Stereoscopic optic nerve photographs were graded in a masked fashion. RESULTS: Ninety-four eyes of 48 healthy individuals, 89 eyes of 55 diabetic patients who did not undergo PRP, and 37 eyes of 24 subjects with diabetes who underwent PRP were included in this study. Eyes that had been treated with PRP had thinner peripapillary RNFL compared with the other groups; this was statistically significantly different in the inferior (P = .004) and nasal (P = .003) regions. Optic nerve cupping did not increase with severity of disease classification, but the proportion of optic nerves graded as suspicious for glaucoma or as having nonglaucomatous optic neuropathy did (P = .008). These grading categories were associated with thinner RNFL measurements. CONCLUSIONS: Diabetic eyes that have been treated with PRP have thinner RNFL than nondiabetic eyes. Optic nerves in eyes treated with PRP are more likely to be graded as abnormal, but their appearance is not necessarily glaucomatous and may be related to thinning of the RNFL.

ABCA4 gene sequence variations in patients with autosomal recessive cone-rod dystrophy.

OBJECTIVE: To identify sequence variations in the ABCA4 gene in a cohort of patients with autosomal recessive cone-rod dystrophy. METHODS: The coding sequences of the ABCA4 gene were analyzed in 30 unrelated probands. In those patients with plausible disease-causing variations, correlations were made between genotype and fundus phenotype as well as with electrophysiological and visual field findings. RESULTS: Sixteen (53%) of 30 probands were found to harbor plausible disease-causing variations in the ABCA4 gene. Two distinctly different fundus phenotypes were observed in our cohort of patients. Twelve patients showed diffuse pigmentary degenerative changes, whereas 4 showed either no pigmentary changes or only a mild degree of peripheral pigment degeneration. An associa-tion between certain sequence variations and each of these 2 different phenotypes was observed. CONCLUSIONS: Our findings confirm that a substantial percentage of patients with autosomal recessive cone-rod dystrophy are likely to harbor a mutation in the ABCA4 gene as the cause of their disease. The fundus phenotype observed in such patients is quite variable, and certain fundus phenotypes may be more associated with certain genotypes. Clinical Relevance Identification of the molecular genetic basis for various inherited human retinal dystrophies, such as cone-rod dystrophy, facilitates a potentially better understanding of the mechanisms by which photoreceptor cells degenerate. This in turn provides guidance as to how to better proceed in identifying the most optimal future therapeutic strategies.

Local proliferation of microglia cells in response to neocortical injury in vitro.

Studies examined whether increased numbers of microglia following neural damage result from induced mitotic activity of resident microglia in situ. Organotypic slice cultures of neocortex were maintained for 1 week prior to placement of lesions. Increased numbers of OX-6 or tomato lectin labeled microglial cells were detected 1-8 days following lesions. Administration of BrdU to the cultures demonstrated lectin and BrdU double labeled microglial cells, conclusively demonstrating that a portion of the microglial cells were generated by local mitotic activity in situ.