13 niðurstöður
Neutral and acid protease activities inhibited by chymostatin, leupeptin, pepstatin and HgCl2 in mononuclear cells and granulocytes showed no significant differences between myotonic dystrophy patients and controls. These results suggest that chymotrypsin and cathepsin B and D activities are
Sarcoplasmic masses contain disorganized myofibrillar material and are a striking feature of myotonic dystrophy. However their significance is still unclear. Using immunocytochemistry we studied the expression of cytoskeletal proteins (desmin and vimentin), dystrophin, markers of myogenic
Recent data suggest that death of muscle cells during development and in selected pathological conditions occurs via apoptosis. We investigated the occurrence of apoptosis in normal and pathological human skeletal muscle, using in situ end-labeling (ISEL) to detect DNA fragmentation, and
Human muscle sarcoplasmic reticulum (SR) yields three major protein bands. The percent distribution of the mean values of the bands from 15 normal human muscles was 55.4, 14.6, and 30.0 for the 100, 55, and 45-kDa mass proteins, respectively. A mean distribution similar to that in normal muscle SR
Activation of Rho-associated protein kinase 1 (ROCK1) and myotonic dystrophy kinase-related CDC42-binding kinase alpha (MRCKα) by caspases during apoptosis in vertebrates represents a prototypical example of co-option of kinases by proteases. How caspases acquired the ability to control these
Transcriptomes provide a myriad of potential RNAs that could be the targets of therapeutics or chemical genetic probes of function. Cell-permeable small molecules, however, generally do not exploit these targets, owing to the difficulty in the design of high affinity, specific small molecules
In the advanced stage of dystrophinopathy, cardiac dysfunction is a serious complication for prognosis. Recently, an angiotensin converting enzyme (ACE), which converts angiotensin (A) 1 to A 2, has been reported to be effective for cardiac insufficiency. The A 2 is produced more dominantly in the
Our studies showed a significantly increased neutral protease activity in mononuclear cells in patients with MS in relapse, active neuro-Behçet's disease, acute disseminated encephalomyelitis (ADEM) and polymyositis. Furthermore, in patients with ADEM there was a significant increase in the
Studies showed a significant decrease in the macrophage neutral protease and lymphocyte acid protease activities in patients with multiple sclerosis in remission, a significantly decreased neutral protease activity in macrophages in patients with myasthenia gravis and a significantly decreased acid
BACKGROUND
Our understanding of the genetic basis of muscle disease has grown dramatically over the last few years. Gene tests are now available for the diagnosis of several conditions and molecular research is providing greater understanding of pathogenesis.
METHODS
This article reviews some of
Insmed is developing mecasermin rinfabate, a recombinant complex of insulin-like growth factor-I (rhIGF-I) and binding protein-3 (rhIGFBP-3) [insulin-like growth factor-I/insulin-like growth factor binding protein-3, rhIGF-I/rhIGFBP-3, SomatoKine], for a number of metabolic and endocrine
The excretion of endogenous creatinine and 3-methylhistidine by subjects with muscle diseases has been measured in order to assess muscle mass and fractional rates of myofibrillar protein degradation. Increases in the rates of myofibrillar protein breakdown were observed in all subjects with
Imaging of collectively invading cocultures of carcinoma cells and stromal fibroblasts reveals that the leading cell is always a fibroblast and that carcinoma cells move within tracks in the extracellular matrix behind the fibroblast. The generation of these tracks by fibroblasts is sufficient to