Abstract: The present invention relates to methods for performing antisense oligonucleotide-mediated exon skipping in the retina of a subject in need thereof. In particular, the present invention relates to a method for performing antisense oligonucleotide-mediated exon skipping in a retina cell of a subject comprising the step of injecting into the vitreous of the subject an amount of the antisense oligonucleotide.

Abstract: The present invention relates to methods for performing antisense oligonucleotide-mediated exon skipping in the retina of a subject in need thereof. In particular, the present invention relates to a method for performing antisense oligonucleotide-mediated exon skipping in a retina cell of a subject comprising the step of injecting into the vitreous of the subject an amount of the antisense oligonucleotide.

Abstract: The present invention relates to a method for treating a Leber congenital amaurosis in a patient harbouring the mutation c.2991+1655 A>G in the CEP290 gene, comprising the step of administering to said patient at least one antisense oligonucleotide complementary to nucleic acid sequence that is necessary for preventing splicing of the cryptic exon inserted into the mutant c. 2991+1655 A>G CEP290 mRNA.

Abstract: 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.

Abstract: The present invention relates to a method for treating a Leber congenital amaurosis in a patient harbouring the mutation c.2991+1655 A>G in the CEP290 gene, comprising the step of administering to said patient at least one antisense oligonucleotide complementary to nucleic acid sequence that is necessary for preventing splicing of the cryptic exon inserted into the mutant c. 2991+1655 A>G CEP290 mRNA.

Abstract: The present invention relates to a method for treating a Leber congenital amaurosis in a patient harbouring the mutation c.2991+1655 A>G in the CEP290 gene, comprising the step of administering to said patient at least one antisense oligonucleotide complementary to nucleic acid sequence that is necessary for preventing splicing of the cryptic exon inserted into the mutant c.2991+1655 A>G CEP290 mRNA.

Abstract: The present invention relates to methods for performing antisense oligonucleotide-mediated exon skipping in the retina of a subject in need thereof. In particular, the present invention relates to a method for performing antisense oligonucleotide-mediated exon skipping in a retina cell of a subject comprising the step of injecting into the vitreous of the subject an amount of the antisense oligonucleotide.

Abstract: The present invention relates to a method for treating a Leber congenital amaurosis in a patient harbouring the mutation c.2991+1655 A>G in the CEP290 gene, comprising the step of administering to said patient at least one antisense oligonucleotide complementary to nucleic acid sequence that is necessary for preventing splicing of the cryptic exon inserted into the mutant c.

Abstract: The present invention relates to a method for treating a Leber congenital amaurosis in a patient harboring the mutation c.2991+1655 A>G in the CEP290 gene, comprising the step of administering to said patient at least one antisense oligonucleotide complementary to nucleic acid sequence that is necessary for preventing splicing of the cryptic exon inserted into the mutant c.2291+1655 A>G CEP290 mRNA.

Abstract: Methods of forming a glass article are disclosed. In one embodiment, a method of forming a glass article includes translating a pulsed laser beam on a glass substrate sheet to form a laser damage region between a first surface and a second surface of the glass substrate sheet. The method further includes applying an etchant solution to the glass substrate sheet to remove a portion of the glass substrate sheet about the laser damage region. The method may further include strengthening the glass substrate sheet by an ion-exchange strengthening process, and coating the glass substrate sheet with an acid-resistant coating. Also disclosed are methods where the laser damage region has an initial geometry that changes to a desired geometry following the reforming of the glass substrate sheet such that the initial geometry of the laser damage region compensates for the bending of the glass substrate sheet.

Abstract: The present invention relates to a method for treating a Leber congenital amaurosis in a patient harbouring the mutation c.2991+1655 A>G in the CEP290 gene, comprising the step of administering to said patient at least one antisense oligonucleotide complementary to nucleic acid sequence that is necessary for preventing splicing of the cryptic exon inserted into the mutant c.

Abstract: The present invention relates to a method for treating a Leber congenital amaurosis in a patient harboring the mutation c.2991+1655 A>G in the CEP290 gene, comprising the step of administering to said patient at least one antisense oligonucleotide complementary to nucleic acid sequence that is necessary for preventing splicing of the cryptic exon inserted into the mutant c.2291+1655 A>G CEP290 mRNA.

Abstract: Methods of forming a glass article are disclosed. In one embodiment, a method of forming a glass article includes translating a pulsed laser beam on a glass substrate sheet to form a laser damage region between a first surface and a second surface of the glass substrate sheet. The method further includes applying an etchant solution to the glass substrate sheet to remove a portion of the glass substrate sheet about the laser damage region. The method may further include strengthening the glass substrate sheet by an ion-exchange strengthening process, and coating the glass substrate sheet with an acid-resistant coating. Also disclosed are methods where the laser damage region has an initial geometry that changes to a desired geometry following the reforming of the glass substrate sheet such that the initial geometry of the laser damage region compensates for the bending of the glass substrate sheet.

Abstract: A method, an apparatus, and a computer program product for wireless communication are provided. The apparatus determines an observed bit rate based on uplink transmissions of the UE, estimates an available link capacity for the UE, selects an estimate factor, and estimates available uplink throughput for future uplink transmissions of the UE as a function of the observed bit rate, the estimated available link capacity, and the estimate factor.

Abstract: The present invention relates to a method for treating a Leber congenital amaurosis in a patient harbouring the mutation c.2991+1655 A>G in the CEP290 gene, comprising the step of administering to said patient at least one antisense oligonucleotide complementary to nucleic acid sequence that is necessary for preventing splicing of the cryptic exon inserted into the mutant c.

Abstract: The present invention relates to a method for treating a Leber congenital amaurosis in a patient harboring the mutation c.2991+1655 A>G in the CEP290 gene, comprising the step of administering to said patient at least one antisense oligonucleotide complementary to nucleic acid sequence that is necessary for preventing splicing of the cryptic exon inserted into the mutant c.2291+1655 A>G CEP290 mRNA.

Abstract: The present invention relates to a method for treating a Leber congenital amaurosis in a patient harbouring the mutation c.2991+1655 A>G in the CEP290 gene, comprising the step of administering to said patient at least one antisense oligonucleotide complementary to nucleic acid sequence that is necessary for preventing splicing of the cryptic exon inserted into the mutant c.

Abstract: Disclosed are novel light polarizing articles comprising a substrate, a light polarizing layer, an inorganic intermediate layer between the polarizing layer and the substrate, an optional inorganic sub-layer between the substrate and the inorganic intermediate layer, and a protective layer over the light polarizing layer, and method of making the same. Due to the presence of the inorganic intermediate layer and the optional sub-layer, adhesion of the polarizing layer is improved substantially. The light polarizing article has improved chemical, mechanical and thermal resistance. The light polarizing article can be used, for example, as ophthalmic products and in display devices.

Abstract: Disclosed are novel light polarizing articles comprising a substrate, a light polarizing layer, an inorganic intermediate layer between the polarizing layer and the substrate, an optional inorganic sub-layer between the substrate and the inorganic intermediate layer, and a protective layer over the light polarizing layer, and method of making the same. Due to the presence of the inorganic intermediate layer and the optional sub-layer, adhesion of the polarizing layer is improved substantially. The light polarizing article has improved chemical, mechanical and thermal resistance. The light polarizing article can be used, for example, as ophthalmic products and in display devices.

Abstract: Disclosed are novel light polarizing articles comprising a substrate, a light polarizing layer, an inorganic intermediate layer between the polarizing layer and the substrate, an optional inorganic sub-layer between the substrate and the inorganic intermediate layer, and a protective layer over the light polarizing layer, and method of making the same. Due to the presence of the inorganic intermediate layer and the optional sub-layer, adhesion of the polarizing layer is improved substantially. The light polarizing article has improved chemical, mechanical and thermal resistance. The light polarizing article can be used, for example, as ophthalmic products and in display devices.