A combined treatment for nerve injury is provided. Accordingly there is provided a composition comprising a hyaluronic acid, a laminin polypeptide, an antioxidant and an anti-gliotic agent. Also provided are matrices and hydrogels of the composition and methods of using same.

A method for preparing powdery superoxide dismutase (SOD) hydrolysates. SOD is hydrolyzed by cellulase and then further hydrolyzed with a solution containing a mixture of proteases. Organic citric acid is added in the SOD hydrolysates solution, then the solution is freeze-dried to obtain the powdery SOD hydrolysates.

Provided are novel human copper-zinc superoxide dismutase, also known as superoxide dismutase 1 or SOD1, specific antibodies as well as fragments, derivatives and variants thereof as well as methods related thereto. Assays, kits, and solid supports related to antibodies specific for SOD1 are also disclosed. The antibody, immunoglobulin chain(s), as well as binding fragments, derivatives and variants thereof can be used in pharmaceutical and diagnostic compositions for SOD1 targeted immunotherapy and diagnosis, respectively.

Provided are a method and system for simultaneously extracting polysaccharides of Rosa roxburghii Tratt, polyphenols of Rosa roxburghii Tratt, superoxide dismutase (SOD) of Rosa roxburghii Tratt, and Vc from Rosa roxburghii Tratt pomace. The method includes enzymatic hydrolysis treatment, grinding treatment, ultrasonic treatment, centrifugation treatment, ceramic membrane ultrafiltration treatment, macroporous adsorption resin treatment, elution treatment, evaporation and concentration treatment, spiral-wound membrane ultrafiltration treatment, and reverse osmosis treatment.

The present invention provides novel methods of cell disruption and release of biomolecules from a cell. The invention comprises the use of positively and/or negatively charged microparticles comprising ground resin. It is particularly useful for purification of biomolecules from cell culture.

This invention presents the method and use of the AAV-XBP1s/GFP virus, in the prevention and treatment of amyotrophic lateral sclerosis, as presented in the in vivo studies in FIG. 6.

The present invention provides a composition and method for treating, delaying the onset, delaying progression of, reducing the incidence of or reducing the severity of amyotrophic lateral sclerosis in a subject. The composition a peptide derived from SOD1 which can be used to inhibit formation of SOD1 amyloid-like aggregates or for production of anti-SOD1 antibodies.

This invention provides a stably transformed plant, plant part and/or plant cell, comprising a heterologous polynucleotide encoding a superoxide reductase (SOR) from an archaeon species, wherein said stably transformed plant, plant cell, and/or plant part has increased disease resistance. The invention further provides a method of increasing disease resistance in a plant, plant cell, or plant part, comprising: introducing into said plant, plant cell, or plant part a heterologous polynucleotide encoding a superoxide reductase from an archaeon species to produce a stably transformed plant, plant cell, or plant part, thereby producing a plant, plant part, or plant cell having increased disease resistance as compared to a control. Additionally provided are plants, plant parts, and plant cells produced by the methods of the invention, as well as progeny and products produced therefrom.

An expression vector containing appropriate mitochondrion-targeting sequences (MTS) and appropriate 3UTR sequences provides efficient and stable delivery of a mRNA encoding a protein (CDS) to the mitochondrion of a mammalian cell. The MTS and 3UTR sequences guide the CDS mRNA from the nuclear compartment of the cell to mitochondrion-bound polysomes, where the CDS is translated. This provides an efficient translocation of a mature functional protein into the mitochondria. A method of targeting mRNA expressed in the nuclear compartment of a mammalian cell to the mitochondrion is also provided. The vector and methods can be used to treat defects in mitochondrial function.

An agent for treating acute respiratory distress syndrome includes, as an active ingredient, a lecithinized superoxide dismutase represented by the general formula (I):

SOD(Q-B).sub.m(I)

(wherein, SOD represents a residue of a superoxide dismutase; Q represents a chemical crosslinking; B represents a residue of lysolecithin, in which a hydrogen atom of a hydroxyl group is removed from the lysolecithin having the hydroxyl group at the 2-position of glycerol; and m is the average number of bonds of the lysolecithin relative to one molecule of the superoxide dismutase and represents an integer of 1 or more).