Acetylcholinesterase (EC3.1.1.7; AChE), an enzyme critical for cholinergic neurotransmission, is abundantly expressed in neurons and mature myotubes, and we recently found that muscle AChE expression was suppressed in parallel with the inhibition of myogenic differentiation upon TCDD treatment in mouse C2C12 cells.
This TCDD-induced suppression of muscle AChE was proposed to involve an aryl hydrocarbon receptor (AhR)-independent mechanism, but the precise underlying mechanism remains unclear.
Differently, Iba-1 is downregulated after axotomy but upregulated after partial lesion of peripheral nerve as well as after virus inoculation and during non-inflammatory muscle pain.
Reduction of muscle AChE activity and biotransformation enzymes ethoxyresorufin-O-deethylase and glutathione S-transferase and antioxidant enzymes such as, SOD and glutathione peroxidase, as well as increased brain DNA damage, coincided with the highest number of tissue lesions in the liver and gills in the spring, regardless of the sampling point.
Changes in maximal voluntary isometric contraction strength (MVC) and muscle soreness, plasma creatine kinase (CK) activity and myoglobin concentration after 80% EC were compared between groups by a mixed-factor ANOVA.
There was an increased risk of adverse events with PDE5 inhibitors, especially headache (OR 1.97, 95% CI 1.33 to 2.92; 5 trials, 848 participants), gastrointestinal upset (OR 1.63, 95% CI 1.07 to 2.48; 5 trials, 848 participants), flushing (OR 4.12, 95% CI 1.83 to 9.26; 3 trials, 748 participants), and muscle aches and joint pains (OR 2.52, 95% CI 1.59 to 3.99; 4 trials, 792 participants).Data comparing PDE5 inhibitors to placebo whilst on other PAH-specific therapy were limited by the small number of included trials.
At baseline, 24 and 48 h, creatine kinase, lactate dehydrogenase, interleukin-6 and -10, tumor necrosis factor alpha, and muscle soreness were assessed.
Our results indicate that the later-onset FMF patients had a lower percentage of MEFV mutations in exon 10 and predominantly presented arthritis and myalgia.
Using repeated intramuscular injection of nerve growth factor to induce the development of sustained muscle pain (lasting weeks), 30 healthy individuals were randomized to receive 5 consecutive daily treatments of active or sham left DLPFC rTMS, starting before the first nerve growth factor injection on day 0.
At Day-0 versus Day-5, the sham compared to active group showed: Higher muscle pain scores and reduced PPTs (P < 0.04); decreased frontal N30 SEP (P < 0.01); increased TMS map volume (P < 0.03).
At Day-0 versus Day-5, the sham compared to active group showed: Higher muscle pain scores and reduced PPTs (P < 0.04); decreased frontal N30 SEP (P < 0.01); increased TMS map volume (P < 0.03).
Gain-of-function mutations in STIM1 or ORAI1 isoforms cause tubular aggregate myopathy (TAM), a skeletal muscle disorder with muscular pain, weakness and cramping.
Anti-interleukin-1 (IL-1) therapy may be a beneficial and a reasonable treatment option, when there is insufficient response to NSAID and corticosteroid therapies in pediatric PFMS patients.
Anti-interleukin-1 (IL-1) therapy may be a beneficial and a reasonable treatment option, when there is insufficient response to NSAID and corticosteroid therapies in pediatric PFMS patients.
Equine myofibrillar myopathy (MFM) causes exertional muscle pain and is characterized by myofibrillar disarray and ectopic desmin aggregates of unknown origin.
SAMS are particularly difficult to treat because there are no validated biomarkers or tests that can be used to confirm patient self-reports of SAMS, and a number of patients who report SAMS have non-specific muscle pain not attributable to statin therapy.
SAMS are particularly difficult to treat because there are no validated biomarkers or tests that can be used to confirm patient self-reports of SAMS, and a number of patients who report SAMS have non-specific muscle pain not attributable to statin therapy.