192 results about "Retinal ganglion cell" patented technology

A method, device and system for stimulating visual tissue, typically in the retina or visual cortex, to achieve an artificial percept of light or image. The method includes providing stimulating electrodes suitable for placement in proximity to the visual tissue and generating a series of short-duration stimulation signals having a duration of less than about 0.5 milliseconds each. The short-duration stimulation signals are applied through the stimulating electrodes with varying frequencies that are substantially matched to a spiking range of frequencies of at least one ganglion cell for perceiving brightness or image.

Embodiments of the invention are directed toward neuroprotective formulations that may prevent the progression of glaucoma by strengthening the resistance of nerve cells to damage. Some embodiments of the invention are directed toward neuroprotective formulations that may limit and prevent glaucomatous damage by blocking the mechanisms that lead to retinal ganglion cell death. Other embodiments of the invention involve specific component formulations and methods of using the formulations.

In vivo imaging may be used to assess a condition (e.g., a state of glaucoma or a state of ocular hypertension) of an eye of a living animal. A dye may be intravenously injected into the living animal. The dye may bind to amyloid in the nervous system of the animal. Images may be taken of a retina, an optic nerve head, an optic nerve, the lateral geniculate nucleus, and/or the visual cortex. Images may be taken using methods such as fluorescent angiography, magnetic resonance imaging, computed tomography, positron emission tomography, and/or single photon emission computed tomography. The condition of the eye and/or retinal ganglion cells in the eye may be assessed from one or more of the images. The condition of the eye may be assessed based on the presence of amyloid in one or more of the images.

The invention discloses an artificial retina implant. The artificial retina implant comprises a receiving coil, a demodulation stimulation module, an electrode array and a loop electrode. The receiving coil is in alignment connection with a transmission coil of an artificial retina in-vitro device and receives image coding signals and energy emitted by the in-vitro device, the demodulation stimulation module is connected with the receiving coil and decodes the image coding signals received by the receiving coil, converts the received image coding signals into electrical signals and transmits the electrical signals to the electrode array, and the received energy is converted. The artificial retina implant can achieve the visual effect only by stimulating retinal ganglion cells of the inner layer, and is easy to implant, safe and reliable.

The invention belongs to the field of pharmaceutical preparations, and relates to a long-acting sustained release preparation for preventing or treating retinal damage, and a preparation method thereof. The long-acting sustained release preparation takes erythropoietin (EPO) as an active component, takes dextran as a protective agent for the active component, and takes poly(lactic-co-glycolic acid), polylactic acid or polycaprolactone as a coating component to prepare sustained release microspheres, wherein the erythropoietin is coated by the poly(lactic-co-glycolic acid), polylactic acid or polycaprolactone. Proven by animal experiments, the sustained release microspheres of the long-acting sustained release preparation provided by the invention have the same protective actions on the ganglionic cells of damaged retinas by single vitreous chamber injection and repeated EPO protein vitreous chamber injection, and the sustained release microspheres are capable of avoiding a series of complications caused by many times of injection and overcoming the defects of repeated intraocular injection administration and gene therapy. The long-acting sustained release preparation provided by the invention adopts intraocular local administration, can reduce the dosage and treatment cost, and can not generate adverse effects on other organs or tissues in vivo.

The invention discloses an artificial retina system which comprises an in-vitro part and an implantation part. The in-vitro part comprises a portable power source, vision glasses and a transmission coil. The portable power source is connected with the vision glasses to provide external power supply for the whole artificial retina system. The vision glasses comprise a camera lens, a main board and an interface board. The transmission coil is connected with a radio frequency modulation module and used for receiving an image coded signal. The implantation part comprises a receiving coil, a demodulation stimulating module and a stimulating electrode. The receiving coil is in alignment connection with the transmission coil. The demodulation stimulating module is connected with the receiving coil, decodes the image coded signal received by the receiving coil and converts the image coded signal into an electric signal to be transmitted to the stimulating electrode. The stimulating electrode comprises a plurality of contact electrodes and electrode wires connected with the contact electrodes one to one. The artificial retina system can directly stimulate retinal ganglion cells on the innermost layer, most electronic devices are arranged on the in-vitro part, and therefore images are updated and processed easily.

The present invention relates to methods of treating or preventing retinal ganglion cell (RGC) death and/or glaucoma using modulators of neurotrophic receptors that comprise β-turn peptidomimetic cyclic compounds or derivatives thereof. The neurotrophic receptor modulators can be used alone, in combination and/or in conjunction with one or more other compounds, molecules or drugs that treat or prevent ocular hypertension, RGC death and/or glaucoma.

Basic ideas of the invention are that through simulating information processing flow of early vision of biologic optic nerve system, designing following items solves certain issues. The said items designed in the invention are: layered network structure of simulating layered information processing mode in biologic optic nerve system; computing unit of imitating nerve ganglion, and its variable distribution of sensing field on sensor layer; computing unit for detecting moving orientation in third layer possessing local stage by stage computing mechanism; alertness algorithm for detecting moving event. The invention makes the designed parts release conflict between computing efficiency, precision and computation resources, as well as makes machine vision system pay attention to first important information, meanwhile keep alertness around.

The invention provides methods for treating ocular diseases using a recombinant vehicle to express a protein useful in the treatment of ocular disease, with particular preference for use of neurotrophin-4 (NT4) for targeting subpopulations of cells in the retina. A genetically engineered gene transfer vector containing sequences encoding a growth factor such as neurotrophin-4 (NT4) is used to transduce cells of the retinal ganglion cell (RGC) layer, in situ, via administration of the vector intravitreally. Accordingly, methods are disclosed for treating subjects in need thereof by therapeutic protein delivery via a recombinant expression vector, including rescue of photoreceptors by targeting the RGC layer subpopulation of retinal cells.

This invention relates to the neuroprotection of the optic nerve and the treatment of glaucoma, more specifically, the invention is directed to a method of preventing, inhibiting, decreasing incidence and suppressing death in ganglion cells by manipulating the P2X₇ and A₃ receptors on ganglion cells, by reducing levels of ATP released into the extracellular space of the retina and enhancing the conversion of released extracellular ATP into adenosine.

The present invention relates to taurine or taurine-like substances for the prevention and treatment of a disease associated with retinal ganglion cell degeneration. More particularly the invention relates to a substance selected from the group consisting of taurine, a taurine precursor, a taurine metabolite, a taurine derivative, a taurine analog and a substance required for the taurine biosynthesis for the prevention and treatment of a disease associated with retinal ganglion cell degeneration.

The present invention provides an isolated nucleic acid molecule comprising, or consisting of, the nucleic acid sequence of SEQ ID NO:1 or a nucleic acid sequence of at least 400 bp having at least 80% identity to said sequence of SEQ ID NO:1, wherein said isolated nucleic acid molecule specifically leads to the expression in direction selective retinal ganglion cells of a gene when operatively linked to a nucleic acid sequence coding for said gene.

Contemplated compositions and methods employ a TGF-beta superfamily protein or antagonist thereof to treat a neural disorder characterized by an imbalance in differentiated functional sensory and neural cells derived from a sensory/neural progenitor cell. Preferably, GDF-11 and/or antagonists thereof are employed in the treatment of diseases in which visual and/or auditory progenitor cells will provide for a repair mechanism to the disease. Most preferably, GDF-11 is employed as a modulator of competency to increase production of retinal ganglion cells, retinal photoreceptors, retinal amacrine cells, sensory hair and supporting cells of the vestibulocochlear epithelium, and/or neurons and supporting cells of the spiral acoustic ganglion and vestibulo-cochlear (auditory) nerve to which it gives rise.

An apparatus for in vivo electroporating a plasmid into a retina of any eye includes a first electrode with a first polarity of voltage placed in contact with a cornea of the eye, a second electrode with an opposite second voltage at least in part behind the retina, and a pulsed voltage source for providing a pulsed DC voltage with an optimized field strength amplitude, frequency, number of pulses, group repetition rate and duration of pulse and group repetition, which are optimized for transfection of the channelrhodospsin-2 (ChR2) gene into the retinal ganglion cells. An in vivo method for treating retinal ganglion cells in an eye without use of viral transfection includes the steps of nonviral in vivo delivering a channelrhodospsin-2 (ChR2) gene to target the specific (retinal ganglion) cells of a retina by intravitreous injection of plasmid DNA, electroporating the plasmid into the retina and use of image intensification device for stimulating the retinal ganglion cells with ambient lighting conditions.

The invention discloses a micro-electrode array chip before retina in the field of artificial vision. The micro-electrode array chip comprises a chip substrate, a lead buried in the chip substrate and micro-electrodes protruding the surface of the substrate and forming an array. The edge of the lower end of the chip substrate is provided with at least two lower suture line preformed holes; a micro-electrode arrangement lower area, a micro-electrode arrangement middle area, a micro-electrode arrangement upper area, a substrate reduction area and a substrate expansion area are sequentially arranged on the chip substrate from bottom to top; the substrate expansion area contains contacts corresponding to the electrode arrangement areas, and are connected with the micro-electrodes through the lead buried in the chip substrate; the chip substrate close to the lower end of the substrate reduction area is provided with at least three groups of two sclera cut suture line preformed holes, and two edges are respectively provided with at least two upper suture line preformed holes; and two sides of the substrate expansion area are provided with eye external suture line preformed holes. The micro-electrode array chip can stimulate retinal ganlion cells of the blind to recover partial vision of the blind, and avoids rhegmatogenous retinal detachment, choroidal hemorrhage and sympathetic ophthalmia caused by iatrogenic retinal breaks.

A lighting apparatus includes a light emitter that emits a first illumination light as a display illumination light. The optical characteristics of the first illumination light are: a correlated color temperature in a range from 3800 K to 6500 K, inclusive; chromaticity deviation Duv in a range from −9 to 0, inclusive; and an intrinsic photosensitive retinal ganglion cell (ipRGC) stimulus level of at least 0.6, the ipRGC stimulus level being a value standardized by setting an ipRGC stimulus level of light emitted from a D65 light source to 1.

A new combined index of structure and function (CSFI) for staging and detecting glaucomatous damage is provided. An observational study including 333 glaucomatous eyes (295 with perimetric glaucoma and 38 with preperimetric glaucoma) and 330 eyes of healthy subjects is described. All eyes were tested with standard automated perimetry (SAP) and spectral domain optical coherence tomography (SDOCT) within 6 months. Estimates of the number of retinal ganglion cells (RGC) were obtained from SAP and SDOCT and a weighted averaging scheme was used to obtain a final estimate of the number of RGCs for each eye. The CSFI was calculated as the percent loss of RGCs obtained by subtracting estimated from expected RGC numbers. The performance of the CSFI for discriminating glaucoma from normal eyes and the different stages of disease was evaluated by receiver operating characteristic (ROC) curves. The mean CSFI, representing the mean estimated percent loss of RGCs, was 41% and 17% in the perimetric and pre-perimetric groups, respectively (P<0.001). They were both significantly higher than the mean CSFI in the normal group (P<Q.0( )1). The CSFI had larger ROC curve areas than isolated indexes of structure and function for detecting perimetric and preperimetric glaucoma and differentiating among early, moderate and advanced stages of visual field loss. An index combining structure and function performed better than isolated structural and functional measures for detection of perimetric and preperimetric glaucoma as well as for discriminating different stages of the disease.

The invention provides a medicine for preventing retinal ganglion oxidative stress. The medicine is a preparation prepared by taking a DNA tetrahedron as an active component and adding pharmaceutically acceptable auxiliary materials or auxiliary components. The invention also provides application of the DNA tetrahedron in preparation of the medicine for preventing oxidative stress of retinal ganglion cells and apoptosis. The tFNA is used for preparing the medicine for preventing oxidative stress of the retinal ganglion cells, is helpful for treating diseases caused by oxidative stress of the retinal ganglion cells such as glaucoma, and has a very good application prospect.

The invention relates to a recombinant adeno-associated virus vector. The recombinant adeno-associated virus vector comprises constitutively active human Nrf2 (Nrf2 (CA)), a CMV promoter/enhancer, beta-globin intron for increasing gene expression, human growth hormone poly (A) tail sequence, etc. The invention also relates to a preparation method of the recombinant adeno-associated virus vector and the application of the recombinant adeno-associated virus vector or a composition containing the recombinant adeno-associated virus vector in preparing a medicine for treating glaucoma retinal ganglion cell denaturation. The recombinant adeno-associated virus vector provided by the invention can obviously reduce the intraocular pressure of a mouse, increase the survival rate of RGCs of the mouse, and effectively treat glaucoma retinal ganglion cell pathological changes.

Microbial type rhodopsins, such as the light-gated cation-selective membrane channel, channelrhodopsin-2 (Chop2/ChR2) or the ion pump halorhodopsin (HaloR) are expressed in retinal ganglion cells upon transduction using recombinant AAV vectors. Selective targeting of these transgenes for expression in discrete subcellular regions or sites is achieved by including a sorting motif in the vector that can target either the central area or surround (off-center) area of these cells. Nucleic acid molecules comprising nucleotide sequences encoding such rhodopsins and sorting motifs and their use in methods of differential expression of the transgene are disclosed. These compositions and methods provide significant improvements for restoring visual perception and various aspects of vision, particular in patients with retinal disease.

The present invention provides a contour detection method based on a non-classical receptive field and linear nonlinear modulation. The method comprises: A, inputting an image to be detected through gray processing; B, performing Gabor filtering of the image to be detected to obtain the Gabor energy value of each direction of each pixel point; C, constructing X-cell and Y-cell simulation models in a retina ganglion cell; D, calculating and obtaining stimulating response of each central neuron through the non-classical receptive field corresponding to the X cell; E, calculating and obtaining the stimulating response of each central neuron through the non-classical receptive field corresponding to the Y cell; F, respectively calculating the stimulating response of central neurons of the X cell and the Y cell through the combined modulation of the classical receptive field and the non-classical receptive field, and performing addition of the stimulating response of central neurons of the X cell and the Y cell to take as a corresponding contour value; and G performing processing of the contour values of each pixel point to obtain a final contour value. The contour detection method based on the non-classical receptive field and the linear nonlinear modulation overcomes the defect that the contour recognition rate is low in the prior art, and has good simulation effect and high contour recognition rate.

A use method of agmatine or a pharmaceutically allowable salt thereof, and a pharmaceutical composition comprising the same are disclosed. The method and pharmaceutical composition of the present invention can effectively cure or prevent eye diseases preferably including glaucoma, retinopathy, and optic neuropathy associated with apoptosis in retinal ganglion cells (RGCs), particularly hypoxia-induced or tumor necrosis factor-α (TNF-α)-induced apoptosis.

Provided herein are compounds of Formula I, compositions comprising an effective amount of a compound of Formula I, and methods for preventing, reducing or treating retinal ganglion cell damage comprising administering an effective amount of a purine derivative to a subject in need thereof.