22 results about "Retinal damage" patented technology

Improved ophthalmic devices including optical sub-elements with custom design for directing images to specific portions of a patient's retina. The optical sub-elements may be used to direct images along a direction divergent from a central axis of the lens base. By redirecting images along divergent directions, ophthalmic devices according to the present invention allow users with specialized needs, such as low light conditions and / or retinal damage to utilize undamaged regions of the retina to have a higher degree of vision capability.

The invention provides a compound for preventing and treating retinal ganglion cytopathy as well as a preparation method and application thereof, and particularly relates to the field of biological medicines. The invention provides a strain of Umbellopsisin A, the Umbellopsisin A metabolized by the Umbellopsisin A can significantly increase the number of viable retinal ganglion cells and also can improve visual conduction dysfunction, and the Umbellopsisin A can effectively pass through a blood retina barrier to achieve efficient prevention of omentum ganglion cell death, so that the Umbellopsisin A can be used for preparing medicines for treating retinal ganglion cell death. And retina injury can be repaired.

The present invention discloses a method for repairing or preventing retinal damage, which includes: administering a composition comprising a Lactobacillus plantarum PL-02 strain or a metabolite thereof to a subject in need thereof; wherein the PL-02 strain is deposited at the China General Microbiological Culture Collection Center with a deposition number CGMCC 20485.

The application provides application of thrombospondin 1 in preparation of a drug for preventing and / or treating retinal injury, and belongs to the technical field of eye disease drugs. The application verifies the anti-inflammatory effect of thrombospondin 1 (THBS-1) in experimental blue light induced retinal inflammation by means of in vitro cell experiments and in vivo animal experiments, and verifies the role of thrombospondin 1 in inhibiting pathological neovascularization and the protective effect on retinal injury. Therefore, the application provides application of thrombospondin 1 in preparation of a drug for preventing and / or treating age-related macular degeneration.

The invention provides application of effective components of guava fruits in eye protection, and belongs to the technical field of biological medicine. The invention provides an application of effective components of guava fruits in preparation of eye protection medicines, an application in preparation of medicines for treating retina light injury and an application in preparation of medicines for inhibiting apoptosis of eye cells. According to the embodiment of the invention, a zebra fish blue light eye injury model and a mouse retina light injury model are constructed and treated by using the effective components of the guava fruits, and the effective components of the guava fruits are found to have a protective effect on eye cell apoptosis, retina injury and the like, and the protective effect of the effective components is equivalent to that of xanthophyll.

This invention discloses the application of disodium 4,4'-diisothiocyanate-2,2'-stilbene sulfonate in the preparation of drugs for the prevention, delay, and / or treatment of blue light-induced retinal damage. It belongs to the field of biomedical technology. This invention demonstrates for the first time that sodium DIDS can effectively protect photoreceptor cells from blue light damage: at the cellular level, sodium DIDS can restore mitochondrial membrane potential, increase ATP levels, reduce reactive oxygen species accumulation, and inhibit mitochondrial-dependent apoptosis; at the animal level, intravitreal injection of sodium DIDS can improve vision in mice exposed to blue light, restore the amplitude of a-waves and / or b-waves in electroretinograms, and protect the outer segment length and outer nuclear layer thickness of cone cells. Sodium DIDS provides a novel therapeutic strategy for blue light-induced retinal photodamage through multi-target synergistic protection of mitochondrial function.

The invention discloses a screen assembly with a skin care effect, and relates to the technical field of display. The screen assembly comprises a display screen and an optical function layer arranged on the display screen. The optical functional layer is configured to perform spectrum modulation on light rays emitted by the display screen; the spectrum modulation comprises the steps of blocking or attenuating harmful light rays of which the wavelengths are within a first preset range, and allowing beneficial light rays of which the wavelengths are within a second preset range to penetrate through, or enhancing the intensity of the beneficial light rays through light conversion. The optical function layer with specific spectral characteristics is integrated in the screen assembly, so that high-energy short-wave blue light is effectively shielded to prevent retina injury and skin oxidation, and meanwhile, long-wave light rays beneficial to skin can be utilized or enhanced; therefore, when a user uses the electronic equipment, the beautifying and protecting effects of promoting collagen generation, resisting aging and the like are realized.

The present invention belongs to the field of pharmaceutical technology, and particularly relates to the application of prostaglandin E2 in the preparation of a medicament for treating retinal damage caused by blue light exposure. The present invention uses a prostaglandin E2 medicament or a pharmaceutical composition to prevent or treat retinal damage caused by blue light exposure. The medicament or the pharmaceutical composition has the function of reducing the shortening of the retinal photoreceptor cell layer and alleviating the decline of the electroretinogram a-wave and b-wave, and thus can improve the pathological changes related to retinal diseases.

The present invention relates to the technical field of visual function detection, specifically a visual function detection method and system based on image analysis, including the following steps: collecting multi-wavelength reflection images of the fundus, adjusting the set wavelength parameters of the light source, activating the imaging device to receive images, denoising and contrast adjusting the collected images, and generating a multi-wavelength retinal image dataset. In the present invention, by collecting multi-wavelength images and performing meticulous denoising processing, the clarity and contrast of the images are significantly improved, bringing higher precision to damage recognition, reducing the chance of misdiagnosis. By calculating the light intensity gradient to map retinal damage, not only the damage range is accurately captured, but also the positioning of the damaged area is refined. The high-speed capture of the pupil dynamic response and its data analysis provide in-depth insights into eye movement patterns, making the evaluation of visual function more intuitive and comprehensive. By cross-verifying the visual field defect and pupil dynamic data, the comprehensiveness and accuracy of the evaluation are enhanced.

The invention discloses a multi-modal sensing Al self-adaptive brightness adjustment low-blue-light head-up display optical system, which is characterized in that a multi-modal data acquisition layer is arranged to fuse environment, vehicle and driver state information, and precise scene recognition is realized through a multi-modal data preprocessing layer and a core AI processing layer; the blue light adjustment decision layer generates an adjustment instruction giving consideration to eye protection, visibility and comfort, and finally the HUD brightness and the blue light content are dynamically adjusted and controlled through the multi-mode execution feedback layer. According to the method, effective suppression of harmful blue light and intelligent adaptation of display brightness in different driving scenes are achieved, the retina injury risk and the human eye adjustment burden caused by long-time use of the HUD are remarkably reduced, and the visual comfort and safety in the driving process are improved.

Limosilactobacillus reuteri subsp. reuteri LR1349 is deposited at the Deutsche Sammlung von Mikroorganismen und Zellkulturen (DSMZ) GmbH under an accession number DSM 35135 in accordance with the Budapest Treaty. A method for alleviating blue light-induced retinal damage using a composition containing Limosilactobacillus reuteri subsp. reuteri LR1349 is also provided. The composition is a food product or a pharmaceutical composition.

Limosilactobacillus reuteri subsp. reuteri LR1349 is deposited at the Deutsche Sammlung von Mikroorganismen und Zellkulturen (DSMZ) GmbH under an accession number DSM 35135 in accordance with the Budapest Treaty. A method for alleviating blue light-induced retinal damage using the same, a composition for use in alleviation of blue light-induced retinal damage, use of a composition in the manufacture of a medication or a food product in alleviation of blue light-induced retinal damage in a subject, and a pharmaceutical composition for alleviation of blue light-induced retinal damage are also provided.

A portable system and method for training a substitute retinal location of an eye of a retinal impaired viewer, and an auxiliary system for improving vision of such a viewer are disclosed. The portable system for training includes an eye tracking module for providing information of the viewer's eye and a virtual image display module for displaying a virtual image at a center of a substitute retinal location on the viewer's impaired retina instead of a center of a fovea. The virtual image display module further includes a first light signal generator for generating a plurality of first light signals and a first combiner for redirecting the plurality of first light signals to the substitute retinal location when a pupil of the viewer's eye is substantially located at a center of the eye.

The invention discloses application of Crx, Nrl and Otx2 in inducing cells to be transdifferentiated into photoreceptor-like cells and a method for preparing the photoreceptor-like cells, the method comprises the step of expressing induction genes in starting cells, and the induction genes are Crx, Nrl and Otx2. Inducing genes Crx, Nrl and Otx2 are expressed in fibroblasts, so that the fibroblasts are transdifferentiated into photoreceptor-like cells, and the photoreceptor-like cells can be automatically migrated and integrated into the retina of a host after being transplanted into the subretinal space of a mouse, so that the damaged retina is repaired. Since a large number of fibroblasts are present in the skin, this makes it possible to treat retinal injury by inducing transdifferentiation of fibroblasts into photoreceptor-like cells on a large scale.

Compositions, nucleic acid molecules and methods for inducing photoreceptor regeneration and for treating retinal damage, disease, and degeneration in mammalian subjects. Such a nucleic acid molecule comprises a nucleic acid sequence encoding a proneural transcription factor (ASCL1 or NEUROD1) and one or more additional transcription factors selected from OTX2, CRX, and RAX. A method for inducing photoreceptor regeneration in a retina comprises administering to a retina the nucleic acid molecule encoding a proneural transcription factor and one or more additional transcription factors, wherein expression of the nucleic acid molecule stimulates regeneration of photoreceptors from retinal Müller glia (MG).

Described herein are compositions and methods for inducing retinal regeneration in a subject. Also described herein are compositions and methods for treating, preventing, reducing the likelihood of having, reducing the severity of, and / or slowing the progression of a retinal degenerative disease, retinal damage, or retinal blindness in a subject. In some embodiments, the compositions and methods may comprise a pharmaceutical composition comprising a Foxp gene expression vector comprising a polynucleotide sequence encoding a Foxp polypeptide, functional variant thereof, or fragment thereof.

Tissue replacement implants are disclosed that include polarized retinal pigment epithelial cells on a poly(lactic-co-glycolic acid) (PLGA) scaffold, wherein the PLGA scaffold is 20-30 microns in thickness, has a DL-lactide / glycotide ratio of about 1:1, an average pore size of less than about 1 micron, and a fiber diameter of about 150 to about 650 nm. Also disclosed are methods of treating a subject with a retinal degenerative disease, retinal or retinal pigment epithelium dysfunction, retinal degradation, retinal damage, or loss of retinal pigment epithelium. These methods include locally administering to the eye of the subject the tissue replacement implant. In further embodiments, methods are disclosed for producing the tissue replacement implant.

The utility model relates to a red light eye protection mask which aims at providing blue light protection for eyes and improving the eye using environment. The eye protection mask is composed of four layers of structures including a base layer, a blue light filtering layer, a spectrum conversion layer and a protection layer. The base layer adopts a transparent polyester film with the thickness of 40-120 microns, the thickness of the blue light filtering layer is 20-80 microns, and a quantum dot material is used for effectively blocking harmful blue light; the thickness of the spectrum conversion layer is 10-30 [mu] m, and quantum dots with the particle size of 5-20 nm convert part of light into red light beneficial to eyes; and the outermost protective layer is an organic silicon coating or a hardened PET film, so that the internal structure is prevented from being damaged and corroded by the outside. According to the red light eye protection mask, the risk of retina injury caused by long-time exposure in front of a screen of electronic equipment is remarkably reduced, eye fatigue is reduced by converting light into long-wave red light, and the visual comfort is improved. In addition, the product does not cause color distortion or brightness reduction, and the original display effect of the screen is kept.

Provided is a bifidobacterium longum strain, selected from the group consisting of BL1363, DSM 35138 and BL531, DSM 35139. A method for alleviating blue light-induced retinal damage, a composition for use in alleviation of blue light-induced retinal damage, use of a composition in the manufacture of a medication or a food product in alleviation of blue light-induced retinal damage in a subject, and a pharmaceutical composition for alleviation of blue light-induced retinal damage with the bifidobacterium longum strain are also provided.

The invention relates to the skipping of the CEP290 exon 36 in an individual suffering from a retinal dystrophy accounted for by a nonsense mutation or a premature termination codon generated by a frameshift mutation in exon 36 or an upstream exon, including the c.4723A>T, c.4771C>T, c.4714G>T, c.4786_4790del, c.4791_4794del, c.4732G>T, c.4625_4626insCATG (35), c.4792_4795del, c.4801C>T, c.4805C>T, or c.4811G>A mutations, to bypass protein truncation and lessen retinal damages. Here, studying fibroblasts from control individuals, and two patients carrying the CEP290 c.4723A>T nonsense mutation, they show low levels of spontaneous skipping of exon 36 arising from both endogenous basal skipping and mutation-induced skipping. The minimally shortened and mutation-free CEP290 mRNA produced by skipping of exon 36 in the fibroblasts of the two patients is translated into a protein isoform that localizes at the centrosome and allows the formation of primary cilia, yet with elongated axonemes. Using an AON consisting of a sequence set forth as SEQ ID NO: 1, complementary to a nucleic acid sequence of CEP290 pre-mRNA, wherein said AON targeting an mRNA encoding the donor splice site (H36D) is capable to alter splicing by blocking the recognition of exon 36 and bypass protein truncation while maintaining the open reading frame, leading to the production of near full-length CEP290 protein, they were able to increase the abundance of the alternatively spliced mRNA and shortened protein and to reduce axonemal length in patient cells.

The present disclosure relates to compositions and methods for treating retinal damage and / or retinal degradation. More specifically, this disclosure relates to methods for treating degradation of the retinal pigment epithelium by administering compositions comprising a nucleoside and / or a nucleoside or nucleotide reverse transcriptase inhibitor.

The invention relates to the field of biomedicine, in particular to application of T21 site mutation of PNP protein in treatment of retina degenerative diseases. According to the invention, a CRISPR-Cas9 technology is used to autonomously construct a mutant with a PNP protein T21 site mutated into alanine. Tests prove that the mutant can improve the retina cell purine metabolism homeostasis, regulate and control the retina microenvironment inflammation level and reduce retina cell structure and function damage, can serve as a target spot to research related medicine for treating retina damage, and provides a new thought and means for treatment of retina degenerative diseases.