The present invention relates to a pharmaceutical composition comprising (i) a compound promoting the expression and/or the activity of one or more long non-coding RNAs (lncRNAs) selected from SEQ ID NOs 12, 8 to 11 and 13; and/or (ii) a compound inhibiting the expression and/or the activity of one or more lncRNAs selected from SEQ ID NOs 1 to 7, 27 and 28. The present invention also relates to a compound (i) promoting the expression and/or the activity of one or more lncRNAs selected from SEQ ID NOs 12, 8 to 11 and 13; and/or (ii) inhibiting the expression and/or the activity of one or more lncRNAs selected from SEQ ID NOs 1 to 7, 27 and 28 for use in treating or preventing cardiac hypertrophy.

The present invention discloses RNAi constructs derived from a Fusarium chitin synthase gene Chs3b, which has a nucleotide sequence as shown by SEQ ID NO: 1. Five distinct RNAi vectors are constructed for 5 different segments of the Chs3b gene (named Chs3b-1, 2, 3, 4, and 5, respectively), and separately transformed into Fusarium. It is found that siRiNAs in the transformed Fusarium shows a significant inhibition in fungal growth, development, and pathogenicity. The expression of the RNAi vectors against Chs3b in plants may inhibit the infection of Fusarium and improve the resistance of the transgenic plants to Fusarium head blight.

Small interfering RNA (siRNA) knock down antisense transcripts, and regulate the expression of their sense partners. This regulation can either be discordant (antisense knockdown results in sense transcript elevation) or concordant (antisense knockdown results in concomitant sense transcript reduction).

Intergenic non-coding RNA molecules that regulate the expression of HWP1 and ALS3 of Candida are provided as are methods of using the non-coding RNA molecules and complementary molecules thereof in modulating HWP1 or ALS3 expression; adherence, yeast-to-hyphal transition, or biofilm development of Candida; and preventing or treating candidiasis.

A method of treating traumatic brain injury (TBI) and other neurological disorders is presented herein. Both conditioned media (CM) containing long non-coding RNAs such as NEAT1 (nuclear enriched abundant transcript 1) and MALAT1 (metastasis associated lung adenocarcinoma transcript 1) as well as human adipose-derived stem cells (hADSCs) themselves (Tx), when administered at least 3 hours post injury, were found to significantly ameliorate motor and cognitive functions in young, but not aged, mice undergoing TBI. Significant reduction in cortical damage and hippocampal cell loss was observed in both Tx and CM groups in young rats, whereas less neuroprotection was detected in the aged rats and mainly in the Tx group but not the CM group, which may in part result from decreased homing of the cells to the spleen.

The oligonucleotide compositions of the present invention make use of combinations of oligonucleotides. In one aspect, the invention features an oligonucleotide composition including at least 2 different oligonucleotides targeted to a target gene. This invention also provides methods of inhibiting protein synthesis in a cell and methods of identifying oligonucleotide compositions that inhibit synthesis of a protein in a cell.

Disclosed are antisense molecules and compositions for the treatment of Staphylococcus aureus infection. The antisense molecules and compositions comprise nucleic acid molecules, such as RNA, DNA, or nucleic acid molecules with modified backbones, such as PNA. The antisense molecules and compositions inhibit expression of membrane stability proteins in Staphylococcus aureus; are optionally conjugated to cell penetration molecules such as peptides; and are optionally administered in the form of a nanoparticle composition.

Disclosed are methods of treating chronic nervous system diseases or injuries, e.g., chronic spinal cord injury, using Nogo receptor antagonists, including Nogo receptor-1 (NgR1) polypeptides, Nogo receptor-1 antibodies and antigen-binding fragments thereof, soluble Nogo receptors and fusion proteins thereof, and polynucleotides. Also disclosed are methods of noninvasively monitoring axonal growth during and after treatment with an axonal growth promoting agent.

RNA interference is provided for inhibition of histamine receptor H1 mRNA expression, in particular, for treating patients having an HRH1-related condition or at risk of developing an HRH1-related condition such as allergic conjunctivitis, ocular inflammation, dermatitis, rhinitis, asthma, or allergy.

The present invention relates to antisense of oligonucleotides that modulate the expression of and/or function of Fibroblast growth factor 21 (FGF21), in particular, by targeting natural antisense polynucleotides of Fibroblast growth factor 21 (FGF21). The invention also relates to the identification of these antisense oligonucleotides and their use in treating diseases and disorders associated with the expression of FGF21.