Night vision

About: Night vision is a research topic. Over the lifetime, 6004 publications have been published within this topic receiving 67372 citations.

Eye safe laser imaging system

Abstract: An active night vision system capable of viewing a target over long distances utilizes laser illumination in eye-safe, invisible wavelength regions of about 1.52 - 1.76 νm or about 2.03 νm - 2.34 νm for illuminating a target; and electronically receives, intensifies and displays or stores the reflected image.

Night vision goggle with separate camera and user output paths

Abstract: A night vision device comprising a first detector, a beam splitter, a user optical output and a camera. The first detector is configured to detect and transmit a scene image in a first spectral band along a first optical path. The beam splitter is configured to receive the first optical path image; to output, along a second optical path, a first portion of the first optical path image, and to output, along a third optical path, a second portion of the first optical path image. The user optical output is configured to receive and output images traveling along the second optical path. The camera is configured to receive and store images traveling along the third optical path.

Fusion of 2- /3- /4-sensor imagery for visualization, target learning, and search

Abstract: We present recent work on methods for fusion of imagery from multiple sensors for night vision capability. The fusion system architectures are based on biological models of the spatial and opponent-color processes in the human retina and visual cortex. The real-time implementation of the dual-sensor fusion system combines imagery from either a low-light CCD camera (developed at MIT Lincoln Laboratory) or a short-wave infrared camera (from Sensors Unlimited, Inc.) With thermal long-wave infrared imagery (from a Lockheed Martin microbolometer camera). Example results are shown for an extension of the fusion architecture to include imagery from all three of these sensors as well as imagery from a mid- wave infrared imager (from Raytheon Amber Corp.). We also demonstrate how the results from these multi-sensor fusion systems can be used as inputs to an interactive tool for target designation, learning, and search based on a Fuzzy ARTMAP neural network.

Residual electroretinograms in young Leber congenital amaurosis patients with mutations of AIPL1.

Abstract: Leber congenital amaurosis (LCA) is a severe congenital or early-onset inherited retinal dystrophy that classically presents with searching nystagmus, absence of normal pupil responses, flat electroretinograms (ERGs), minimal, if any, vision beyond infancy, and an initially normal fundus appearance, followed by the development of pigmentary changes over time. The term LCA has traditionally been used when these features present within the first 6 months of life, whereas a variety of terms such as juvenile retinitis pigmentosa,1 early childhood onset retinitis pigmentosa,2 or severe early childhood onset retinal dystrophy (SECORD)3 have been used to describe milder forms of the disease that present after 1 year. LCA and SECORD are genetically extremely heterogeneous, and are caused by >16 genes (AIPL1, CEP290, CRX, CRB1, GUCY2D, IMPDH1, IQCB1, LCA5, LRAT, MERTK, RD3, RDH12, RPGRIP1, RPE65, SPATA7, and TULP1). All except CRX and IMPDH1 exhibit autosomal recessive inheritance in which some de novo mutations result in an autosomal dominant trait.3–5 The gene AIPL1 encodes aryl hydrocarbon receptor interacting protein-like 1 (AIPL1), a 384-amino acid protein with three tetratricopeptide repeat motifs. AIPL1 has been suggested to play a role in photoreceptor development6 and protein farnesylation7 and as a chaperone for NUB1, Hsp70, Hsp90, and photoreceptor-specific phosphodiesterases (PDE6β).8–12 Although AIPL1 was initially thought to be expressed only in adult rod photoreceptors,13 its expression in adult rodent cones has now been demonstrated.14 Mutations in AIPL1 are estimated to account for approximately 5% to 10% of all cases of LCA.4,15 Patients usually have severe vision loss (ranging from 20/200 to LP), but milder forms that would fit the definition of a later onset rod-cone dystrophy have also been reported.2,16–19 Other typical features include poorly responsive pupils, nystagmus, hyperopia, and unrecordable ERGs. The fundus appearance in patients with AIPL1 mutations can appear normal early in the disease, but most patients eventually demonstrate a pigmentary retinopathy with a high prevalence of macular atrophy. One series demonstrated that cataracts and keratoconus were common in those with homozygous AIPL1 mutations.18 Spectral domain-optical coherence tomography (SD-OCT) has shown severe loss of outer retinal thickness in the macula, lamellar disorganization, and increased inner retinal thickness.16 Successful gene replacement therapy in AIPL1-deficient mouse models has raised the hope that such methods could be translated for human treatment.20,21 However, Jacobson et al.16 recently studied the feasibility of treatment in a series of patients with AIPL1 mutations and concluded that the severe photoreceptor degeneration seen might mean they were not good candidates for gene replacement therapy unless and that evidence would be needed in much younger patients of some photoreceptor preservation. We herein report three young patients with mutations in AIPL1 who presented with the clinical features of LCA but had residual electroretinograms characterized by slow insensitive scotopic responses and absent photopic responses. The presence of these residual ERG responses potentially indicated greater photoreceptor preservation than seen in older patients and suggested that these patients might be better candidates for gene replacement therapy than previously considered.

The molecular origin and evolution of dim-light vision in mammals

Abstract: The nocturnal origin of mammals is a longstanding hypothesis that is considered instrumental for the evolution of endothermy, a potential key innovation in this successful clade. This hypothesis is primarily based on indirect anatomical inference from fossils. Here, we reconstruct the evolutionary history of rhodopsin--the vertebrate visual pigment mediating the first step in phototransduction at low-light levels--via codon-based model tests for selection, combined with gene resurrection methods that allow for the study of ancient proteins. Rhodopsin coding sequences were reconstructed for three key nodes: Amniota, Mammalia, and Theria. When expressed in vitro, all sequences generated stable visual pigments with λMAX values similar to the well-studied bovine rhodopsin. Retinal release rates of mammalian and therian ancestral rhodopsins, measured via fluorescence spectroscopy, were significantly slower than those of the amniote ancestor, indicating altered molecular function possibly related to nocturnality. Positive selection along the therian branch suggests adaptive evolution in rhodopsin concurrent with therian ecological diversification events during the Mesozoic that allowed for an exploration of the environment at varying light levels.