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muscular atrophy/betændelse
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A severe mouse model of spinal muscular atrophy develops early systemic inflammation.
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Spinal muscular atrophy (SMA) is a fatal genetic disease, mainly affecting children. A number of recent studies show, aside from lower motor neuron degeneration and atrophy of skeletal muscles, widespread defects present in the central nervous system (CNS) and peripheral non-neuronal cell types of
Cytokine profiles in multifocal motor neuropathy and progressive muscular atrophy.
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Multifocal motor neuropathy (MMN) and progressive muscular atrophy (PMA) are associated with IgM monoclonal gammopathy or the presence IgM anti-GM1-antibodies. To further investigate the pathophysiology of MMN and PMA we determined concentrations of 16 mainly B-cell associated inflammatory markers
[Immunocytochemical analysis of the inflammatory infiltrate in inclusion body myositis and other neuromuscular disorders with rimmed vacuoles].
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Among 1400 muscle biopsies, we found 16 cases with rimmed vacuoles whose diagnosis were sporadic inclusion body myositis (IBM) (4 cases), juvenile spinal muscular atrophy (6 cases), distal myopathies (3 cases), limb-girdle muscular dystrophy (2 cases), and peripheral neuropathy (1 case). Monoclonal
Time course of cigarette smoke-induced changes of systemic inflammation and muscle structure.
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It has become more evident that long-term cigarette smoking (LTCS) has an important extrapulmonary toxicity. The aim of the study was to investigate the time-dependent effects of cigarette smoke exposure on exercise capacity, markers of systemic inflammation, and skeletal muscle structure.
Serum cytokine and chemokine profiles in patients with juvenile muscular atrophy of distal upper extremity (Hirayama disease).
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Juvenile muscular atrophy of the distal upper extremity (Hirayama disease) is characterized by adolescent-onset muscular weakness of the distal upper limb. Several studies showed the contribution of atopic disposition and hyperIgEaemia to the disease process, but it has not been well clarified. To
Inflammatory myopathy with severe tongue atrophy in Pembroke Welsh Corgi dogs.
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A disease characterized by tongue and facial muscle atrophy has been recognized sporadically among Pembroke Welsh Corgi (PWC) dogs in Japan. The present study describes the pathologic findings of this canine syndrome. Histopathologic examinations were performed in 2 dogs, including a case of
Motor neuron degeneration in a 20-week male fetus: spinal muscular atrophy type 0.
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BACKGROUND
Neuropathological changes in degenerating motor neurons are well documented in the term neonate with spinal muscular atrophy, but not at midgestation.
METHODS
Postmortem neuropathological examination was performed in a 20-week male fetus with a hypoplastic left cardiac
Expression of Human Endogenous Retrovirus-K in Spinal and Bulbar Muscular Atrophy.
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Background: Spinal and Bulbar Muscular Atrophy (SBMA) is caused by the extension of the polyglutamine tract within the androgen receptor (AR) gene, and results in a multisystem presentation, including the degeneration of lower motor neurons. The androgen receptor (AR) is known to modulate the
Secondary radiological findings of osteoid osteoma as muscular atrophy and synovitis in paediatric and adult patients
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Purpose: Diagnosis of osteoid osteoma may be delayed if secondary radiological findings such as muscle atrophy, oedema in peripheric soft tissue and bone marrow, joint effusion, or synovitis are more severe than the lesion itself. In this
Neuro-inflammation as a therapeutic target in amyotrophic lateral sclerosis.
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Amyotrophic lateral sclerosis (ALS) is a rapidly progressive neuromuscular disease that destroys both upper and lower motor neurons, resulting in spasticity, diffuse muscular atrophy, weakness, and ultimately death from respiratory failure. It is presumed that in the vast majority of cases, ALS is
Common pathways of autoimmune inflammatory myopathies and genetic neuromuscular disorders.
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It has been shown that many hereditary motor neuron diseases are caused by mutation of RNA processing enzymes. Survival of motor neuron 1 (SMN1) is well-known as a causative gene for spinal muscular atrophy (SMA) and mutations of glycyl- and tyrosyl-tRNA synthetases are identified as a cause of
Chronic inflammatory demyelinating polyradiculoneuropathy with diffuse and massive peripheral nerve hypertrophy: distinctive clinical and magnetic resonance imaging features.
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We present 3 patients with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) with extensive and diffuse hypertrophy of the nerve roots and peripheral nerves. They exhibited slowly progressive sensory impairment and distally predominant limb weakness and muscular atrophy, and markedly
[Sports in patients with systemic inflammatory musculoskeletal diseases].
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Local and systemic inflammatory mechanisms and immobilisation, perhaps secondarily intensified by corticosteroid treatment, very often produce reduced load capacity of the tissues. Pain, swelling of the joints, muscular atrophy and instability favour such development. Increased activity of the
Muscle apoptosis in humans occurs in normal and denervated muscle, but not in myotonic dystrophy, dystrophinopathies or inflammatory disease.
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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
[Sporadic case of non-progressive neurogenic muscular atrophy localized in both calf muscles].
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A 60-year-old woman was admitted to our hospital because of difficulty in standing on her toes. Neurological examination showed muscle weakness in both calf muscles. Her serum creatine kinase (CK) level was slightly elevated. MRI revealed hyper-intense signals localized in both the gastrocnemius and
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