Abstract: A method of inhibiting an overactive fibroblast growth factor receptor 3 (FGFR3) in a cell by contacting the cell with a composition that contains an effective amount of Pheophorbide a, Pyropheophorbide a, or an active derivative thereof. Also disclosed is a method for treating a disorder associated with an overactive FGFR3 with a composition containing an effective amount of Pheophorbide a, Pyropheophorbide a, or an active derivative thereof. Further, a composition for treating a disorder associated with an overactive FGFR3 is described. The composition contains an ethanol extract of Amaranthus viridis.

Abstract: A method of inhibiting an overactive fibroblast growth factor receptor 3 (FGFR3) in a cell by contacting the cell with a composition that contains an effective amount of Pheophorbide a, Pyropheophorbide a, or an active derivative thereof. Also disclosed is a method for treating a disorder associated with an overactive FGFR3 with a composition containing an effective amount of Pheophorbide a, Pyropheophorbide a, or an active derivative thereof. Further, a composition for treating a disorder associated with an overactive FGFR3 is described. The composition contains an ethanol extract of Amaranthus viridis.

Abstract: The disclosure relates, in general, to Glycogen Storage Disease and, in particular, to a method of treating Glycogen Storage Disease and to compounds and compositions suitable for use in such a method.

Abstract: The disclosure relates, in general, to Glycogen Storage Disease Type VI and, in particular, to a method of treating Glycogen Storage Disease Type VI and to compounds and compositions suitable for use in such a method.

Abstract: Methods of treating glycogen storage disease type II, by administering acid ?-glucosidase, are described, as are compositions for use in treatment of glycogen storage disease type II.

Abstract: Described is a method of diagnosing, treating, or monitoring a treatment for Kawasaki disease in a subject. The method includes detecting the level of a biomarker in a sample obtained from the subject, the biomarker being IL-7F, sCD40L, MPIF-1, E-selectin, IP-10, or IL-33. The level is compared to a cut-off level. Also described is a kit for carrying out the method.

Abstract: Methods of treating glycogen storage disease type II, by administering acid ?-glucosidase, are described, as are compositions for use in treatment of glycogen storage disease type II.

Abstract: The disclosure relates, in general, to Glycogen Storage Disease and, in particular, to a method of treating Glycogen Storage Disease and to compounds and compositions suitable for use in such a method.

Abstract: The disclosure relates, in general, to Glycogen Storage Disease and, in particular, to a method of treating Glycogen Storage Disease Type IX and to compounds and compositions suitable for use in such a method, including acid alpha-glucosidase.

Abstract: A method of inhibiting an overactive fibroblast growth factor receptor 3 (FGFR3) in a cell by contacting the cell with a composition that contains an effective amount of Pheophorbide a, Pyropheophorbide a, or an active derivative thereof. Also disclosed is a method for treating a disorder associated with an overactive FGFR3 with a composition containing an effective amount of Pheophorbide a, Pyropheophorbide a, or an active derivative thereof. Further, a composition for treating a disorder associated with an overactive FGFR3 is described. The composition contains an ethanol extract of Amaranthus viridis.

Abstract: Methods of treating glycogen storage disease type II, by administering acid ?-glucosidase, are described, as are compositions for use in treatment of glycogen storage disease type II.

Abstract: The disclosure relates, in general, to Glycogen Storage Disease and, in particular, to a method of treating Glycogen Storage Disease and to compounds and compositions suitable for use in such a method.

Abstract: Methods of treating glycogen storage disease type II, by administering acid ?-glucosidase, are described, as are compositions for use in treatment of glycogen storage disease type II.

Abstract: The disclosure relates, in general, to Glycogen Storage Disease and, in particular, to a method of treating Glycogen Storage Disease and to compounds and compositions suitable for use in such a method.

Abstract: Described herein is a method of determining lithium responsiveness in a bipolar disorder patient. The method includes obtaining a sample from a patient having bipolar disorder, and assaying the sample for the presence or absence of one or more glutamate decarboxylase-like 1 (GADL1) gene variants selected from the group consisting of a T allele of the single nucleotide polymorphism (SNP) rs17026688, a G allele of the SNP rs17026651, and GADL1 1VS8+48delG. The presence of one or more of the GADL1 gene variants indicates that the patient is responsive to lithium treatment.

Abstract: Described is a method of diagnosing, treating, or monitoring a treatment for Kawasaki disease in a subject. The method includes detecting the level of a biomarker in a sample obtained from the subject, the biomarker being IL-7F, sCD40L, MPIF-1, E-selectin, IP-10, or IL-33. The level is compared to a cut-off level. Also described is a kit for carrying out the method.

Abstract: The present invention provides a method of predicting the risk of a patient for developing adverse drug reactions, particularly SJS or TEN. It was discovered that an HLA-B allele, HLA-B* 1502, is associated with SJS/TEN that is induced by a variety of drugs. The correlation with HLA-B* 1502 is most significant for carbamazepine-induced SJS/TEN, wherein all the patients tested have the HLA-B* 1502 allele. In addition, another HLA-B allele, HLA-B*5801, is particularly associated with SJS/TEN induced by allopurinol. Milder cutaneous reactions, such as maculopapular rash, erythema multiforme (EM), urticaria, and fixed drug eruption, are particularly associated with a third allele, HLA-B *4601. For any of the alleles, genetic markers (e.g., HLA markers, microsatellite, or single nucleotide polymorphism markers) located between DRB1 and HLA-A region of the specific HLA-B haplotype can also be used for the test.

Abstract: An anti-granulysin antibody, or an scFv or Fab fragment thereof, capable of binding to an epitope region from R64 to R113 of granulysin and capable of neutralizing an activity of granulysin. The antibody may contain a sequence selected from the sequences of SEQ ID NO:82 to SEQ ID NO:195, or the antibody may contain a sequence selected from the sequences of SEQ ID NO:39 to SEQ ID NO:76. The antibody may be a monoclonal antibody. A method for treating or preventing an unwanted immune response disorder includes administering to a subject in need thereof an effective amount of an anti-granulysin antibody capable of neutralizing the activity of granulysin. The unwanted immune response disorder may be SJS, TEN, or GVHD.

Abstract: Methods of treating glycogen storage disease type II, by administering acid ?-glucosidase, are described, as are compositions for use in treatment of glycogen storage disease type II.

Abstract: Methods of treating glycogen storage disease type II, by administering acid ?-glucosidase, are described, as are compositions for use in treatment of glycogen storage disease type II.