Abstract: Anti-angiogenic treatments, treatments of hyperpermeability disorders, treatments of neuropathic and neurodegenerative disorders, pain treatments, methods of reducing the risk of pre-eclampsia and compounds for use in such methods are described.

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: Anti-angiogenic treatments, treatments of hyperpermeability disorders, treatments of neuropathic and neurodegenerative disorders, pain treatments, methods of reducing the risk of pre-eclampsia and compounds for use in such methods are described.

Abstract: The invention provides VEGFxxxb, or an agent which selectively promotes the expression of VEGFxxxb in preference to VEGFxxx in cells of a subject or in vitro, or an expression vector system which causes the expression of the VEGFxxxb in a host organism, for use in treating or preventing neuropathic and neurodegenerative disorders, or for use as a neuroprotective or neuroregenerative agent in vivo or in vitro. The VEGFxxxb is preferably VEGF165b.

Abstract: A method of detecting a risk of a pregnant female mammal developing pre-eclampsia or a complication linked thereto, or of a fetus of the pregnant female mammal developing a fetal or neonatal deficiency linked to maternal pre-eclampsia, comprises detecting the level of a VEGFxxxb in a sample from the pregnant female mammal at less than about 24 weeks of gestation and comparing the detected level with a reference level. A reduced level in the sample from the pregnant female mammal is indicative of a risk of the pregnant female mammal developing pre-eclampsia or a complication linked thereto or of the fetus developing the fetal or neonatal deficiency linked to maternal pre-eclampsia.

Abstract: The invention provides VEGFxxxb, or an agent which selectively promotes the expression of VEGFxxxb in preference to VEGFxxx in cells of a subject or in vitro, or an expression vector system which causes the expression of the VEGFxxxb in a host organism, for use in treating or preventing microvascular hyperpermeability disorders, or in regulating the pro-angiogenic pro-permeability properties of VEGFxxx isoforms, or in supporting epithelial cell survival without increased permeability, or in reducing the nature (for example the number density and/or size) of fenestrations of epithelial filtration membranes in vivo or in vitro.

Abstract: A method of detecting a risk of a pregnant female mammal developing pre-eclampsia or a complication linked thereto, or of a fetus of the pregnant female mammal developing a fetal or neonatal deficiency linked to maternal pre-eclampsia, comprises detecting the level of a VEGFxxxb in a sample from the pregnant female mammal at less than about 24 weeks of gestation and comparing the detected level with a reference level. A reduced level in the sample from the pregnant female mammal is indicative of a risk of the pregnant female mammal developing pre-eclampsia or a complication linked thereto or of the fetus developing the fetal or neonatal deficiency linked to maternal pre-eclampsia.

Abstract: The invention provides VEGFxxxb, or an agent which selectively promotes the expression of VEGFxxxb in preference to VEGFxxx in cells of a subject or in vitro, or an expression vector system which causes the expression of the VEGFxxxb in a host organism, for use in treating or preventing neuropathic and neurodegenerative disorders, or for use as a neuroprotective or neuroregenerative agent in vivo or in vitro. The VEGFxxxb is preferably VEGF165b.

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.