The present invention relates to nucleic acids of the general formula (I): (N.sub.uG.sub.lX.sub.mG.sub.nN.sub.v).sub.a and derivatives thereof as an immunostimulating agent/adjuvant and to compositions containing same, optionally comprising an additional adjuvant. The present invention furthermore relates to a pharmaceutical composition or to a vaccine, each containing nucleic acids of formula (I) above and/or derivatives thereof as an immunostimulating agent, and optionally at least one additional pharmaceutically active component, e.g. an antigenic agent. The present invention relates likewise to the use of the pharmaceutical composition or of the vaccine for the treatment of cancer diseases, infectious diseases, allergies and autoimmune diseases etc. Likewise, the present invention includes the use of nucleic acids of the general formula (I): (N.sub.uG.sub.lX.sub.mG.sub.nN.sub.v).sub.a and/or derivatives thereof for the preparation of a pharmaceutical composition for the treatment of such diseases.

Disclosed herein are antisense compounds and methods for selectively reducing expression of an allelic variant of a gene containing a single nucleotide polymorphism (SNP). Such methods, compounds, and composition are useful to treat, prevent, or ameliorate diseases, including neurodegenerative diseases, such as Huntington's Disease (HD).

Provided is the use of as SUMF2 gene therapy target for preventing and/or treating an allergic asthma attack and reducing airway hyperresponsiveness. It is verified that the abnormal metabolic pathway of SUMF1/GAG causes epithelial cells to produce a similar immune memory and the epithelial cells can promote T.sub.H2 response when exposed to allergens again. In the present disclosure, SUMF2 gene in airway epithelial cells from a mouse is overexpressed using the adeno-associated virus vector 20 days before the induction of asthma. Compared with a control group, the present disclosure can significantly improve the lung airway inflammation in an asthmatic mouse. Therefore, the overexpression of SUMF2 can be used as a gene therapy target to prevent allergic asthma and reduce airway hyperresponsiveness. Therefore, the use of an adeno-associated virus to overexpress SUMF2 for the prevention of allergic asthma has broad use values and market prospects.

Provided is the use of as SUMF2 gene therapy target for preventing and/or treating an allergic asthma attack and reducing airway hyperresponsiveness. It is verified that the abnormal metabolic pathway of SUMF1/GAG causes epithelial cells to produce a similar immune memory and the epithelial cells can promote T.sub.H2 response when exposed to allergens again. In the present disclosure, SUMF2 gene in airway epithelial cells from a mouse is overexpressed using the adeno-associated virus vector 20 days before the induction of asthma. Compared with a control group, the present disclosure can significantly improve the lung airway inflammation in an asthmatic mouse. Therefore, the overexpression of SUMF2 can be used as a gene therapy target to prevent allergic asthma and reduce airway hyperresponsiveness. Therefore, the use of an adeno-associated virus to overexpress SUMF2 for the prevention of allergic asthma has broad use values and market prospects.

Described herein are cyclic amide-containing pyridyl-xanthines and pharmaceutical compositions thereof that are usesful as antagonists of A.sub.2B adenosine receptors.

The present invention relates to methods and materials for modulating the complement alternative pathway (CAP), the complement classical pathway (CCP), the complement lectin/mannose pathway (CMP), or combinations thereof, as well as methods and materials for targeting diagnostic, prophylactic and therapeutic agents to localized areas of tissue within the body where they may more directly exert their effects upon the intended target cells or tissue, with reduced, associated systemic effects compared with administration of the same or similar agents in an untargeted, systemic manner. The methods and materials of the present invention may therefore allow for increased efficacy, lower threshold effective dosages and/or lower effective maintenance doses, and/or reduced associated undesired or adverse effects in terms of frequency or severity of occurrence, or both. The present invention also relates to methods and materials for modulating a host humoral immune response, especially reducing, inhibiting, or preventing a host humoral immune response.

The invention relates to a novel use of ultrafine nanoparticles, of use as a diagnostic, therapeutic or theranostic agent, characterized by their mode of administration via the airways. The invention is also directed toward the applications which follow from this novel mode of administration, in particular for imaging the lungs, and the diagnosis or prognosis of pathological pulmonary conditions. In the therapeutic field, the applications envisioned are those of radiosensitizing or radioactive agents for radiotherapy (and optionally curietherapy), or for neutron therapy, or of agents for PDT (photodynamic therapy), in particular for the treatment of lung tumors.

The present invention provides means and methods for treating Interleukin 18 (IL-18)-associated diseases and disorders. In particular, the present invention discloses antibodies specific for free IL-18 and IL-18 Binding Protein (IL-18BP) for use in such treatments and for the diagnosis of the indications.

The subject invention provides therapeutic compositions and uses thereof for improving pulmonary function. In one embodiment, the therapeutic composition comprises one or more free amino acids selected from lysine, glycine, threonine, valine, tyrosine, aspartic acid, isoleucine, tryptophan, asparagine, and serine; and electrolytes. In one embodiment, the subject invention can be used to prevent or treat long-term lung complications induced by radiation.

A compound of formula (I) or a pharmaceutically acceptable salt, or N-oxide thereof and the use of the same in therapy: wherein Z, Y, R.sup.1, W, V, and R.sup.3 are as defined in claim 1. ##STR00001##