Abstract: The invention provides a method of selectively pro-oranti-angiogenic treatment of a mammalian subject, comprising site-specific control of alternative splicing during processing of VEGF pre-mRNA transcribed from the C terminal exon 8 of the VEGF gene using controlling agents for the splicing, wherein one or more controlling agent which favors proximal splice site (PSS) splicing in said processing is used in the pro-angiogenic treatment and one or more controlling agent which favors distal splice site (DSS) splicing in said processing is used in the anti-angiogenic treatment.

Abstract: The invention provides a method of selectively pro-oranti-angiogenic treatment of a mammalian subject, comprising site-specific control of alternative splicing during processing of VEGF pre-mRNA transcribed from the C terminal exon 8 of the VEGF gene using controlling agents for the splicing, wherein one or more controlling agent which favours proximal splice site (PSS) splicing in said processing is used in the pro-angiogenic treatment and one or more controlling agent which favours distal splice site (DSS) splicing in said processing is used in the anti-angiogenic treatment.

Abstract: The present invention relates to a molecular motor actin binding protein, in particular, to Nuclear Myosin I&bgr; (NMI&bgr;) containing a 16 amino acid N-terminal extension involved in transcription. More particularly, this invention is directed to a molecule with oligonucleotide sequence coding for a protein nuclear Myosin I&bgr; (NMI&bgr;) containing a 16 amino acid N-terminal extension that co-localizes with, and forms functional complexes with, RNA polymerase II. This invention is also directed to polyclonal and monoclonal antibodies to the 16 amino acid N-terminal extension that block in vitro RNA synthesis. This invention is also directed to administration to a cell of polyclonal or monoclonal antibodies to the NMI&bgr; 16 amino acid N-terminal extension sequence or to an epitope within that sequence to inhibit transcription. Other inhibitors are also suitable. This invention may be used to treat illness through targeted inhibition of cell proliferation.

Abstract: The present invention relates to a molecular motor actin binding protein, in particular, to Nuclear Myosin I &bgr; (NMI &bgr;) containing a 16 amino acid N-terminal extension involved in transcription. More particularly, this invention is directed to a molecule with oligonucleotide sequence coding for a protein nuclear Myosin I &bgr; (NMI &bgr;) containing a 16 amino acid N-terminal extension that co-localizes with, and forms functional complexes with, RNA polymerase II. This invention is also directed to polyclonal and monoclonal antibodies to the 16 amino acid N-terminal extension that block in vitro RNA synthesis. This invention is also directed to administration to a cell of polyclonal or monoclonal antibodies to the NMI &bgr; 16 amino acid N-terminal extension sequence or to an epitope within that sequence to inhibit transcription. Other inhibitors are also suitable. This invention may be used to treat illness through targeted inhibition of cell proliferation.

Abstract: The present invention relates to a molecular motor actin binding protein, in particular, to Nuclear Myosin I&bgr; (NMI&bgr;) containing a 16 amino acid N-terminal extension involved in transcription. More particularly, this invention is directed to a molecule with oligonucleotide sequence coding for a protein nuclear Myosin I&bgr; (NMI&bgr;) containing a 16 amino acid N-terminal extension that co-localizes with, and forms functional complexes with, RNA polymerase II. This invention is also directed to polyclonal and monoclonal antibodies to the 16 amino acid N-terminal extension that block in vitro RNA synthesis. This invention is also directed to administration to a cell of polyclonal or monoclonal antibodies to the NMI&bgr; 16 amino acid N-terminal extension sequence or to an epitope within that sequence to inhibit transcription. Other inhibitors are also suitable. This invention may be used to treat illness through targeted inhibition of cell proliferation.

Abstract: This method of removal of irregularities and highly defected regions of the surface of crystals and epitaxial layers of GaN and Ga1−x−yAlxInyN characterized by mechano-chemical polishing on the soft polishing pad under pressure in presence of chemical etching agent of water solution of bases of the total concentration above 0.01N in time longer than 10 seconds after which the agent is replaced by the pure water without interruption of the polishing and polishing by at least 1 minute aid subsequent diminution of the load and stopping of the machine and then the polished GaN crystal or GaAlInN epitaxial layer is removed of the polishing machine and dried in the stream of dry nitrogen.