A method of reducing pain and induce/enhance the stem cell growth/differentiation reaction includes identifying a pair of related Noxipoints on an identified muscle/organ and applying a chemical/electrical stimulation to the pair of Noxipoints.

The present invention discloses immunomodulating compositions. More particularly, the present invention discloses compositions comprising an immune-modulating agent and a lectin-interactive agent, which are useful for stimulating and prolonging host immune cell responses. The compositions of the present invention are particularly useful in the treatment and/or prophylaxis of a range of conditions including pathogenic infections, autoimmune diseases, transplant rejection, graft versus host disease, allergies, inflammatory disease, as well as cancers and tumors.

The present invention discloses immunomodulating compositions. More particularly, the present invention discloses compositions comprising an immune-modulating agent and a lectin-interactive agent, which are useful for stimulating and prolonging host immune cell responses. The compositions of the present invention are particularly useful in the treatment and/or prophylaxis of a range of conditions including pathogenic infections, autoimmune diseases, transplant rejection, graft versus host disease, allergies, inflammatory disease, as well as cancers and tumors.

The invention provides stabilized aqueous pharmaceutical etanercept compositions suitable for long-term storage of etanercept, methods of manufacture of these compositions, methods of administration, and kits containing same.

The invention provides for a RANKL-specific antagonistic agent recognizing human platelet-expressed receptor activator of nuclear factor kappa-B ligand (pRANKL), for use in treating a cancer patient to prevent or reduce premetastatic lesions in blood.

Pharmaceutical compositions and methods for enhancing targeting of therapeutic compounds to, inter alia, the CNS applied via intranasal administration while reducing non-target exposure are provided. In certain embodiments, at least one vasoconstrictor is provided intranasally prior to intranasal administration of at least one therapeutic compound. In other embodiments, the vasoconstrictor(s) and therapeutic compound(s) are combined in a pharmaceutical composition and delivered intranasally. The present invention substantially increases targeting of the therapeutic compound(s) to, inter alia, the CNS while substantially reducing unwanted and potentially harmful systemic exposure. The preferred administration of the invention applies the vasoconstrictor(s) and/or therapeutic compound(s) to the upper third of the nasal cavity, though application to the lower two-thirds of the nasal cavity is also within the scope of the invention.

Pharmaceutical compositions and methods for enhancing targeting of therapeutic compounds to, inter alia, the CNS applied via intranasal administration while reducing non-target exposure are provided. In certain embodiments, at least one vasoconstrictor is provided intranasally prior to intranasal administration of at least one therapeutic compound. In other embodiments, the vasoconstrictor(s) and therapeutic compound(s) are combined in a pharmaceutical composition and delivered intranasally. The present invention substantially increases targeting of the therapeutic compound(s) to, inter alia, the CNS while substantially reducing unwanted and potentially harmful systemic exposure. The preferred administration of the invention applies the vasoconstrictor(s) and/or therapeutic compound(s) to the upper third of the nasal cavity, though application to the lower two-thirds of the nasal cavity is also within the scope of the invention.

The influence of TF, endothelial cell protein C receptor (EPCR) and protease activated receptor-1 (PAR1) on tumor growth of malignant pleural mesothelioma (MPM) is disclosed. MPM cells that lack or express TF, EPCR or PAR1 and a murine orthotopic model of MPM led to the discovery that intrapleural administration into nude mice of REN MPM cells expressing TF and PAR1 but lacking EPCR and PAR2 generated large pleural cavity tumors. Suppression of TF or PAR1 expression markedly reduced tumor growth. Overexpression of TF in non-aggressive MPM cells expressing EPCR and PAR1 but exhibiting minimal levels of TF failed to alter their tumorigenicity. Introduction of EPCR expression in aggressive MPM cells attenuated tumor growth whereas EPCR silencing in non-aggressive MPM cells overexpressing TF increased tumorigenicity of non-aggressive cells. Expression of EPCR by MPM cells suppresses tumor growth and treats MPM.

The present invention relates to a p75NTR neurotrophin binding protein, p75NTR(NBP), for use in the treatment of pain and/or a symptom of pain.

The present invention relates to a formulation in which glycolipids and phospholipids, isolated from rice bran gum samples, were used in conjunction with gene carrying lipids to test its efficacy in delivering genes to cancer cells selectively. This formulation did not mediate efficient delivery of genes to non-cancerous cells, thus, showing potential use of this formulation to deliver anticancer therapeutics to cancer cells without eliciting treatment related toxicity to normal cells.