muramidase has been researched along with Peripheral-Nervous-System-Diseases* in 2 studies
1 review(s) available for muramidase and Peripheral-Nervous-System-Diseases
| Article | Year |
|---|---|
Ostertag revisited: the inherited systemic amyloidoses without neuropathy.
Mutations in a number of plasma proteins, including transthyretin, apolipoprotein AI, fibrinogen Aalpha-chain, lysozyme, and apolipoprotein AII, are associated with hereditary systemic amyloidosis. Transthyretin amyloidosis is the most common and is usually associated with peripheral neuropathy. Mutations in the other proteins usually have no neuropathic consequences and, instead, cause principally renal and cardiac amyloidosis. Only the apolipoprotein AI glycine 26 arginine mutation may cause peripheral neuropathy and then in only some of the kindreds with this disease. This review is concerned with the non-neuropathic hereditary systemic amyloidoses. It strives to present a synopsis of the present day knowledge of these diseases including each feature of each precursor protein and its mutations; the clinical phenotype of the disease; and suggestions for treatment when feasible. The main objective is to increase awareness of these autosomal dominant diseases, enhance the chances of early diagnosis, enhance the physician's and subsequently the patient's knowledge of each disease, and finally emphasize the need for more research to find ways to treat or prevent these diseases. Topics: Amyloidosis, Familial; Apolipoprotein A-I; Apolipoprotein A-II; Diagnosis, Differential; Fibrinogen; Humans; Muramidase; Mutation; Peripheral Nervous System Diseases | 2005 |
1 other study(ies) available for muramidase and Peripheral-Nervous-System-Diseases
| Article | Year |
|---|---|
In vitro degradation of amyloid material by four proteases in tissue of a patient with familial amyloidotic polyneuropathy.
The effects of 4 proteolytic enzymes, alpha-chymotrypsin, bromeline, collagenase, and lysozyme on amyloid tissue sections from a patient with familial amyloidotic polyneuropathy (FAP) were evaluated. Degradation of amyloid fibrils was significant with alpha-chymotrypsin, moderate with bromeline and collagenase, and slight with lysozyme. All of these proteases except collagenase are used as oral mucolytics in humans. The possibility of their clinical usefulness in the treatment or prevention of the development of FAP is discussed. Topics: Amyloid; Amyloidosis; Bromelains; Chymotrypsin; Humans; In Vitro Techniques; Kidney; Microbial Collagenase; Muramidase; Peptide Hydrolases; Peripheral Nervous System Diseases | 1988 |