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CROSS-REFERENCE TO RELATED APPLICATIONS This application claims the priority benefit of U.S. Provisional Application No.
60/646,818, filed Jan. 25, 2005, and U.S. Provisional Application No. 60/661,688, filed Mar. 14, 2005, both of which are incorporated by reference herein in their entireties. BACKGROUND 1.
Field of the Invention The present invention relates generally to optical therapies and phototherapies for treatment of diseases and physiological disorders, such as, for example, rhinitis. Background of Invention Phototherapy has been used to treat skin disorders, such as psoriasis and atopic dermatitis. As the understanding of the pathophysiologic mechanisms of disease has become better understood, it has been learned that psoriasis is mediated by an immune reaction orchestrated by activated T-cells specific for an antigen. It has also been learned that the T cells undergo apoptosis (or programmed cell death) in response to ultraviolet light therapy (see, for example, Ozawa et al, 312-Nanometer Ultraviolet B Light (Narrow-Band UVB) Induces Apoptosis of T Cells within Psoriatic Lesions, 189(4) J. 711-18, which is incorporated by reference herein). Ultraviolet-B (UVB) light, generally in the range of about 280 nm to about 320 nm, has also been shown to induce cytokines such as interleukin 10 (IL10) and tumor necrosis factor alpha (TNF-α) (see, for example, Narrow-Band Ultraviolet B and Broad-Band Ultraviolet A Phototherapy in Adult Atopic Eczema: A Randomized Controlled Trial, 357 Lancet 2012-16 (2001), which is incorporated by reference herein).
Ultraviolet therapy was also studied in the context of atopic dermatitis and was found to have a beneficial effect (see, for example, Narrow-Band Ultraviolet B and Broad-Band Ultraviolet A Phototherapy in Adult Atopic Eczema: A Randomized Controlled Trial, 357 Lancet 2012-16 (2001) and UVB Phototherapy of Atopic Dermatitis, 119 British Journal of Dermatology 697-705 (1988), both of which are incorporated by reference herein). Similar mechanistic actions of ultraviolet light are invoked in atopic dermatitis as in psoriasis; that is, apoptosis of immune regulatory cells.
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Additional mechanisms are invoked for atopic dermatitis as well. For example, Guhl, et al., (Bivalent Effect of UV Light on Human Skin Mast Cells—Low-Level Mediator Release at Baseline but Potent Suppression upon Mast Cell Triggering, 124 J. 453-56 (2005), which is incorporated by reference,) showed that mast cells from skin are sensitive to UVA light having a wavelength in the range of 320 nm to 400 nm, and that these wavelengths (albeit at higher doses) can inhibit the degranulation of mast cells, thereby preventing histamine release. More recent work in atopic dermatitis has revealed that light concentrated in the blue range (which is generally light having a wavelength in the range of about 400 nm to about 450 nm) can also improve the symptomatology of atopic dermatitis. See, for example, Krutman, et al., Ultraviolet-Free Phototherapy, 21 Photodermatology, Photoimmunology, and Photomedicine 59-61 (2005), which is incorporated by reference. Krutman, et al. Showed that the application 40 J/cm 2 of essentially blue light can dramatically improve the symptomatology of atopic dermatitis even when one observes patients further out over time.
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