This document provides methods and materials involved in identifying and treating autoimmune GFAP (glial fibrillary acidic protein) astrocytopathy, a novel meningoencephalomyelitis, in humans as well as methods and materials for identifying and offering early treatment for patients having autoimmune GFAP astrocytopathy whose autoantibody profile predicts a high likelihood of having underlying cancer (e.g., adenocarcinoma or teratoma).

The invention provides a source of sodium thiosulfate via the dialysate used to cleanse the bool of toxic and metabolic waste in the patients undergoing hemodialysis, peritoneal dialysis, or gastro-intestinal dialysis for treatment of end-stage or near end-stage chronic renal disease. In the method of the invention, dialysis solution components contain therapeutic amounts of sodium thiosulfate, which when fully reconstituted for use as a single solution, deliver 20-130 mg/dl of dialysate.

The invention provides a source of sodium thiosulfate via the dialysate used to cleanse the bool of toxic and metabolic waste in the patients undergoing hemodialysis, peritoneal dialysis, or gastro-intestinal dialysis for treatment of end-stage or near end-stage chronic renal disease. In the method of the invention, dialysis solution components contain therapeutic amounts of sodium thiosulfate, which when fully reconstituted for use as a single solution, deliver 20-130 mg/dl of dialysate.

A method, including a computer-implemented method, is provided for in vivo detection of epidermal growth factor receptor (EGFR) mutation status within peritumoral edematous tissue of a patient. The method includes performing quantitative pattern analysis of magnetic resonance imaging (MRI) data corresponding to MRI of in vivo peritumoral edematous tissue to determine a level of spatial heterogeneity or similarity within the in vivo peritumoral edematous tissue. EGFR mutation status is assigned as one of negative or positive based on the level of spatial heterogeneity or similarity determined. A non-transitory computer-readable storage medium and a system are also provided.

Provided are methods for slowing, halting, and reversing gray matter atrophy and progression of disability in certain neurodegenerative diseases, including multiple sclerosis, using estrogen, alone or in combination with another agent.

Provided are methods for slowing, halting, and reversing gray matter atrophy and progression of disability in certain neurodegenerative diseases, including multiple sclerosis, using estrogen, alone or in combination with another agent.

Provided herein are adipose mimic compositions for use in MRI. The compositions of the invention mimic the MRI properties of human adipose tissue, including T1 relaxation kinetics, T2 relaxation kinetics, magnetic susceptibility, and chemical shift artifact. The compositions of the invention are readily manufactured from inexpensive materials. The compositions of the invention may be used in MRI system calibration or for implementing image correction techniques such as fat suppression.

Described herein are methods for the treatment of cognitive impairment in a subject with a neurological autoimmune disease and methods for determining whether a subject who has a central nervous system autoimmune disease is likely to acquire a cognitive impairment.

Described herein are methods for the treatment of cognitive impairment in a subject with a neurological autoimmune disease and methods for determining whether a subject who has a central nervous system autoimmune disease is likely to acquire a cognitive impairment.

Pre-conditioning a vaccine site with a potent recall antigen such as tetanus/diphtheria (Td) toxoid can significantly improve the lymph node homing and efficacy of tumor antigen-specific DC vaccines. Patients given Td had enhanced DC migration bilaterally and significantly improved survival. In mice, Td pre-conditioning also enhanced bilateral DC migration and suppressed tumor growth in a manner dependent on the chemokines CCL3 and CCL21 and Td-activated CD4.sup.+ T cells. Interference with any component of this axis markedly reduced Td-mediated DC migration and antitumor responses. Our clinical studies and corroborating investigations in mice suggest that pre-conditioning with a potent recall antigen represents a viable strategy to increase DC homing to lymph nodes and improve antitumor immunotherapy.