Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Botulinum toxin A (BoNT-A) is a potent biological toxin widely used for the management of skeletal muscle spasticity or dynamic joint contracture. Intramuscular injection of BoNT-A causes muscle denervation, paresis, and atrophy. This clinical effect of botulinum toxin A lasts 3 to 6 months, and injected muscle eventually regains muscle mass and recovers muscle function. The goal of the present study was to characterize the molecular and cellular mechanisms leading to neuromuscular junction (NMJ) regeneration and skeletal muscle functional recovery after BoNT-A injection. Fifty-six 1-month-old Sprague-Dawley rats were used. Botulinum toxin A was injected into the left gastrocnemius muscle at a dosage of 6 units/kg body weight. An equivalent volume of saline was injected into the right gastrocnemius muscle to serve as control. The gastrocnemius muscle samples were harvested from both hind limbs at 3 days, 7 days, 15 days, 30 days, 60 days, 90 days, 180 days, and 360 days after administration of toxin. In addition, the gastrocnemius muscles from 1-month-old rats with no injections were harvested to serve as uninjected control group. Muscle samples were processed and mRNA was extracted. Real-time polymerase chain reaction (PCR) and gene microarray technology were used to identify key molecules involved in NMJ stabilization and muscle functional recovery. More than 28,000 rat genes were analyzed and approximately 9000 genes are expressed in the rat gastrocnemius muscle. Seven days following BoNT-A injection, 105 genes were upregulated and 59 genes were downregulated. Key molecules involved in neuromuscular junction (NMJ) stabilization and muscle functional recovery were identified and their time course of gene expression following BoNT-A injection were characterized. This animal study demonstrates that following intramuscular injection of BoNT-A, there is a sequence of cellular events that eventually leads to NMJ stabilization, remodeling, and myogenesis and muscle functional recovery. This recovery process is divided into two stages (aneural and neural) and that the IGF-1 signaling pathway play a central role in the process.
 ...
PMID:How muscles recover from paresis and atrophy after intramuscular injection of botulinum toxin A: Study in juvenile rats. 1660 9

Chronic alcoholic myopathy occurs in 40-60% of patients who abuse alcohol, and is accompanied by decreased performance, proximal paresis and atrophy of skeletal muscles. However, it is unknown what is important in the development of the disease: duration of alcohol abuse, or the dose of ethanol consumed. Unknown dynamics of the pathological process in skeletal muscle. We examined male patients identified with alcoholic myopathy and without it, evaluated the duration of alcohol abuse, intake of ethanol, morphological characteristics m.quadriceps vastus lateralis and the content of IGF-1 in plasma. It has been shown that chronic alcoholic myopathy develops after 10 years of alcohol abuse; proximal paresis is observed only in patients with atrophy of muscle fibers, thus there is a transformation of myosin phenotype from slow to fast. The decrease IGF-1 in plasma detected at the early stages of the Church, including in patients without clinical manifestations of proximal paresis and morphological signs of atrophy of muscle fibers.
 ...
PMID:[The Development of Clinical and Morphological Manifestations of Chronic Alcoholic Myopathy in Men with Prolonged Alcohol Intoxication]. 2685 89