Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026850 (muscular dystrophy)
 5,870 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

EPIX is developing MS-325 (AngioMARK), an intravascular magnetic resonance contrast agent for use in the imaging of blood vessels and blood flow in patients with cardiovascular disease, including peripheral vascular disease (PVD). In June 1999, EPIX and Mallinckrodt began phase III trials of MS-325 for the detection of aortoiliac occlusive disease in patients with PVD or abdominal aortic aneurysm [328640]. NDAs for the peripheral and cardiac applications were expected in 1999 and 2000, respectively [275240], [325717]. MS-325 has also shown promise in demonstrating the presence of microscopic muscular dystrophy, as well as monitoring the effects of gene therapy in a mouse model of the disease [360974]. MS-325 is a stable complex of gadolinium and an organic chelating agent. It resembles approved agents in terms of stability, safety and elimination profile, but possesses novel chemical groups which allow it to bind reversibly to albumin. This retains the agent in the blood and, via a patented biophysical phenomenon, enhances the magnetic properties of the gadolinium ion approximately ten-fold.
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PMID:MS-325 EPIX. 1124 2

TGF-beta regulates many aspects of cellular performance relevant to tissue morphogenesis and homeostasis. Postnatal perturbation of TGF-beta signaling contributes to the pathogenesis of many disease states, as recently exemplified through the study of Marfan syndrome (MFS), including aortic aneurysm and skeletal muscle myopathy. Heterogeneity in the regulation and consequences of TGF-beta signaling, amplified in the context of disease, has engendered confusion and controversy regarding its utility as a therapeutic target. Three studies recently published in the JCI, including one in this issue, underscore the complexity of this subject. Heydemann and colleagues implicate dimorphic variation in latent TGF-beta-binding protein 4 (LTBP4), a regulator of TGF-beta bioavailability and activation, as a modifier of muscular dystrophy in gamma-sarcoglycan-deficient mice. In contrast to experience with ascending aortic aneurysm in MFS, Wang and colleagues show that systemic abrogation of TGF-beta signaling worsens (rather than attenuates) Ang II-induced abdominal aortic aneurysm progression in mice. Tieu and colleagues define alterations in the regulation of vascular inflammation in the pathogenesis of Ang II-induced aneurysm and dissection in mice, which may help shed some light on this apparent paradox.
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PMID:TGF-beta in the pathogenesis and prevention of disease: a matter of aneurysmic proportions. 2010 Oct 93