Abstract: The invention relates to nucleic acid molecules for pseudouridylation of a target uridine in a target RNA in a mammalian cell, wherein the nucleic acid molecule comprises a guide region capable of forming a partially double stranded nucleic acid complex with the target RNA comprising the target uridine, wherein the partially double stranded nucleic acid complex is capable of engaging a mammalian pseudouridylation enzyme, wherein the guide region assists in positioning the target uridine in the partially double stranded nucleic acid complex for it to be converted to a pseudouridine by the mammalian pseudouridylation enzyme.

Abstract: The invention relates to nucleic acid molecules for pseudouridylation of a target uridine in a target RNA in a mammalian cell, wherein the nucleic acid molecule comprises a guide region capable of forming a partially double stranded nucleic acid complex with the target RNA comprising the target uridine, wherein the partially double stranded nucleic acid complex is capable of engaging a mammalian pseudouridylation enzyme, wherein the guide region assists in positioning the target uridine in the partially double stranded nucleic acid complex for it to be converted to a pseudouridine by the mammalian pseudouridylation enzyme.

Abstract: The invention relates to antisense oligonucleotides that are capable of bringing about specific editing of a target nucleotide (adenosine) in a target RNA sequence in a eukaryotic cell, wherein said oligonucleotide does not, in itself, form an intramolecular hairpin or stem-loop structure, and wherein said oligonucleotide comprises a non-complementary nucleotide in a position opposite to the nucleotide to be edited in the target RNA sequence.

Abstract: The invention relates to antisense oligonucleotide that are capable of bringing about specific editing of a target nucleotide (adenosine) in a target RNA in a eukaryotic cell, wherein said oligonucleotide does not, in itself, form an intramolecular hairpin or stem-loop structure, and wherein said oligonucleotide comprises a cytidine (a non-complementary nucleotide) or a uridine in a position opposite to the target adenosine to be edited in the target RNA region.

Abstract: An antisense oligonucleotide (AON) capable of inhibiting ADAR-mediated deamination of a target adenosine present in an editing-site sequence (ESS) of a target RNA molecule, wherein under physiological conditions the ESS would hybridize with an editing-site complementary sequence (ESCS) of an RNA molecule to form a double stranded RNA complex, wherein the AON comprises a sequence configured to compete with the ESCS for hybridization with the ESS.

Abstract: The invention relates to antisense oligonucleotides that are capable of bringing about specific editing of a target nucleotide (adenosine) in a target RNA in a eukaryotic cell, wherein said oligonucleotide does not, in itself, form an intramolecular hairpin or stem-loop structure, and wherein said oligonucleotide comprises a cytidine (a non-complementary nucleotide) or a uridine in a position opposite to the target adenosine to be edited in the target RNA region.

Abstract: The invention relates to single-stranded RNA editing antisense oligonucleotides (AONs) for binding to a target RNA molecule for deaminating a target nucleotide, preferably an adenosine, present in the target RNA molecule and recruiting, in a cell, preferably a human cell, an enzyme with nucleotide deamination activity, preferably an ADAR enzyme, to deaminate the target nucleotide in the target RNA molecule. The AONs carry at least one methylphosphonate-modified internucleosidic linkage on a position that would render the AON more stable in comparison to an AON not carrying that methylphosphonate modification at that position.

Abstract: The invention relates to the fields of medicine and immunology. In particular, it relates to novel antisense oligonucleotides (AONs) that may be used in the treatment, prevention and/or delay of Usher syndrome type II and/or USH2A-associated non syndromic retina degeneration.

Abstract: The invention relates to single-stranded RNA editing antisense oligonucleotides (AO Ns) for binding to a target RNA molecule for deaminating at least one target adenosine present in the target RNA molecule and recruiting, in a cell, preferably a human cell, an ADAR2 enzyme, to deaminate the at least one target adenosine in the target RNA molecule. The AON according to the invention comprises a cytidine analog at the position opposite the target adenosine, wherein the cytidine analog serves as an H-bond donor at the N3 site, for more efficient RNA editing.

Abstract: The disclosed computer-implemented method includes determining that an image is to be blurred. The image has multiple pixels arranged along horizontal and/or vertical axes. The method next includes identifying a boundary size for a sliding window within which pixel values are to be sampled from the image and sampling, from pixels that lie on an axis that is diagonal relative to the horizontal/vertical axis of the image, various pixel values from within the boundary of the sliding window. The pixels sampled along the diagonal angle within the sliding window are selected according to a specified noise pattern. The method further includes performing an initial convolution pass on the pixels surrounding the sampled pixels to blur at least some of the pixels surrounding the sampled pixels, and then presenting the blurred image. Various other methods, systems, and computer-readable media are also disclosed.

Abstract: The invention relates to double stranded oligonucleotide complexes comprising an antisense oligonucleotide (AON) and a complementary sense oligonucleotide (SON), for use in the deamination of a target adenosine in a sense target RNA sequence in a cell by an ADAR enzyme, wherein at least the nucleotide in the AON that is directly opposite the target adenosine in the target RNA sequence does not have a 2?-O-alkyl modification and the SON comprises nucleotides that are at least complementary to all nucleotides in the AON that do not have a 2?-O-alkyl modification. The invention further relates to methods of RNA editing using the AON/SON complexes of the invention.

Abstract: The invention relates to the fields of medicine and immunology. In particular, it relates to novel antisense oligonucleotides that may be used in the treatment, prevention and/or delay of Usher Syndrome type II and/or USH2A-associated non syndromic retina degeneration, especially by skipping a pseudo exon (PE40) between exon 40 and 41 in the human USH2A gene.

Abstract: The disclosed computer-implemented method includes determining that an image is to be blurred. The image has multiple pixels arranged along horizontal and/or vertical axes. The method next includes identifying a boundary size for a sliding window within which pixel values are to be sampled from the image and sampling, from pixels that lie on an axis that is diagonal relative to the horizontal/vertical axis of the image, various pixel values from within the boundary of the sliding window. The pixels sampled along the diagonal angle within the sliding window are selected according to a specified noise pattern. The method further includes performing an initial convolution pass on the pixels surrounding the sampled pixels to blur at least some of the pixels surrounding the sampled pixels, and then presenting the blurred image. Various other methods, systems, and computer-readable media are also disclosed.

Abstract: The invention relates to antisense oligonucleotides that are capable of bringing about specific editing of a target nucleotide (adenosine) in a target RNA in a eukaryotic cell, wherein said oligonucleotide does not, in itself, form an intramolecular hairpin or stem-loop structure, and wherein said oligonucleotide comprises a cytidine non-complementary, nucleotide) or a uridine in a position opposite to the target adenosine to be edited in the target RNA region.

Abstract: The invention relates to the fields of medicine and immunology. In particular, it relates to novel antisense oligonucleotides that may be used in the treatment, prevention and/or delay of Usher Syndrome type II and/or USH2A-associated non syndromic retina degeneration, especially by skipping a pseudo exon (PE40) between exon 40 and 41 in the human USH2Agene.

Abstract: The invention relates to antisense oligonucleotides that are capable of bringing about specific editing of a target nucleotide (adenosine) in a target RNA sequence in a eukaryotic cell, wherein said oligonucleotide does not, in itself, form an intramolecular hairpin or stem-loop structure, and wherein said oligonucleotide comprises a non-complementary nucleotide in a position opposite to the nucleotide to be edited in the target RNA sequence.

Abstract: The invention relates to antisense oligonucleotides that are capable of bringing about specific editing of a target nucleotide (adenosine) in a target RNA in a eukaryotic cell, wherein said oligonucleotide does not, in itself, form an intramolecular hairpin or stem-loop structure, and wherein said oligonucleotide comprises a cytidine (a non-complementary nucleotide) or a uridine in position opposite to the target adenosine to be edited in the target RNA region.

Abstract: The invention relates to editing oligonucleotides (EONs) that carry 2?-0-methoxyethyl (2?-MOE) ribose modifications at specified positions and that do not carry such modifications on positions that would lower RNA editing efficiency. The selection of positions that should or should not carry a 2?-MOE modification is based on computational modelling that revealed steric clashes between the 2?-MOE modification and mammalian ADAR enzymes.

Abstract: The invention relates to antisense oligonucleotides that are capable of bringing about specific editing of a target nucleotide (adenosine) in a target RNA sequence in a eukaryotic cell, wherein said oligonucleotide does not, in itself, form an intramolecular hairpin or stem-loop structure, and wherein said oligonucleotide comprises a non-complementary nucleotide in a position opposite to the nucleotide to be edited in the target RNA sequence.

Abstract: The invention relates to nucleic acid molecules for pseudouridylation of a target uridine in a target RNA in a mammalian cell, wherein the nucleic acid molecule comprises a guide region capable of forming a partially double stranded nucleic acid complex with the target RNA comprising the target uridine, wherein the partially double stranded nucleic acid complex is capable of engaging a mammalian pseudouridylation enzyme, wherein the guide region assists in positioning the target uridine in the partially double stranded nucleic acid complex for it to be converted to a pseudouridine by the mammalian pseudouridylation enzyme.