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cardiolipin/fatigue

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文章临床试验专利权
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This study examined 328 CFS sera in a study with 17 CCFP, 8 Gulf War Veterans (GWV), 24 Prostate Cancer (PC), and 52 normal sera in the modified Membrane Immunobead Assay (MIA) procedure for CTX. Three hundred and twenty-eight CFS patients' sera were examined by the modified MIA with purified
Metabolic profiling studies have recently indicated dysfunctional mitochondria in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). This includes an impaired function of pyruvate dehydrogenase complex (PDC), possibly driven by serum factor(s), which leads to inadequate adenosine

Mitochondrial ultrastructural adaptations in fast muscles of mice lacking IL15RA.

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The pro-inflammatory cytokine interleukin-15 (IL15) and its receptor α (IL15RA) participate in the regulation of musculoskeletal function and metabolism. Deletion of the Il15ra gene in mice increases spontaneous activity, improves fatigue resistance in the glycolytic extensor digitorum longus (EDL)
Moyamoya disease is a rare chronic cerebrovascular occlusive disease diagnosed by angiogram with primary features consisting of bilateral occlusion of the internal carotid arteries and of the vessels forming the circle of Willis, and subsequent development of small collateral vessels. These

Sjögren's syndrome: an autoimmune disorder with otolaryngological involvement.

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Sjorgen's syndrome (SS) is an autoimmune exocrinopathy characterized by lymphocyte infiltration of salivary and lacrimal glands that leads to progressive xerostomia and xerophtalmia. One-third of patients suffer of systemic manifestations including arthritis, fever, fatigue and mucosal dryness
A 37-year-old Caucasian woman presented with subacute, symmetrical inflammatory arthralgia, which was affecting her work. Apart from fatigue, she had no other constitutional symptoms. She had undergone cosmetic bilateral silicone breast implant surgery in 2008. Blood tests revealed erythrocyte
Barth syndrome (BTHS) is a rare, X-linked, mitochondrial disorder caused by mutations in the gene encoding tafazzin. BTHS results in cardiomyopathy, muscle fatigue, and neutropenia in patients. Tafazzin is responsible for remodeling cardiolipin, a key structural lipid of the inner mitochondrial
OBJECTIVE To assess the prevalence of extrahepatic manifestations in Bulgarian patients with chronic hepatitis C virus (HCV) infection and identify the clinical and biological manifestations associated with cryoglobulinemia. METHODS The medical records of 136 chronically infected HCV patients were

Efficacy and safety of infliximab in active SLE: a pilot study.

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Tumour necrosis factor-alpha (TNF-alpha) plays a major role in propagating the inflammatory processes responsible for tissue damage in systemic lupus erythematosus (SLE) and is overexpressed both systemically and locally in this disease. Hence, this pilot study was carried out to assess the safety
Tafazzin is a mitochondrial enzyme that exchanges fatty acids between phospholipids by phospholipid-lysophospholipid transacylation. The reaction alters the molecular species composition and, as a result, the physical properties of lipids. In vivo, the most important substrate of tafazzin is the
The presence of antibodies to cardiolipin (ACL Abs) has been reported in some patients suffering from multiple sclerosis (MS), especially of the "neuromyelitic" type. In addition, bright T2-imaging foci (unidentified bright objects) are occasionally detected on brain magnetic resonance imaging (MRI)

Barth syndrome.

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First described in 1983, Barth syndrome (BTHS) is widely regarded as a rare X-linked genetic disease characterised by cardiomyopathy (CM), skeletal myopathy, growth delay, neutropenia and increased urinary excretion of 3-methylglutaconic acid (3-MGCA). Fewer than 200 living males are known
Mitochondria are cell substructures (organelles) critical for cell life, because biological fuel production, the ATP synthesis by oxidative phosphorylation, occurs in them driven by acidity (pH) gradients. Mitochondria play a key role as well in the cell death and in various fatigue and exercise

Cardiac and skeletal muscle defects in a mouse model of human Barth syndrome.

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Barth syndrome is an X-linked genetic disorder caused by mutations in the tafazzin (taz) gene and characterized by dilated cardiomyopathy, exercise intolerance, chronic fatigue, delayed growth, and neutropenia. Tafazzin is a mitochondrial transacylase required for cardiolipin remodeling. Although
The autoimmune/inflammatory syndrome induced by adjuvants (ASIA) is an entity that includes different autoimmune conditions observed after exposure to an adjuvant. Patients with undifferentiated connective tissue disease (UCTD) present many signs and symptoms of ASIA, alluding to the idea that an
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