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muscular atrophy/nekrose
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Digital necrosis in an infant with severe spinal muscular atrophy.
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Resolution of skin necrosis after nusinersen treatment in an infant with spinal muscular atrophy.
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Abnormal motoneuron migration, differentiation, and axon outgrowth in spinal muscular atrophy.
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The role of heterotopic (migratory) motoneurons (HMN) in the pathogenesis of spinal muscular atrophy (SMA) is still controversial. We examined the occurrence and amount of HMN in spinal cord tissue from eight children with SMA (six with SMA-I and two with SMA-II). All affected subjects were carrying
[Clinico-morphologic parallels in aseptic necrosis of the head of the femur in adults].
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The authors reviewed clinical findings from 57 adult patients with aseptic necrosis of the head of the femur. A statistical processing of the findings showed a significant direct correlation between the stages of the process and the degree of femoral muscular atrophy, degree of internal rotation and
Upper motor neurone and descending tract pathology in bovine spinal muscular atrophy.
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The extent of neuropathology in a recently reported disease of Brown Swiss cattle, spinal muscular atrophy (SMA), was investigated with light and electron microscopy. Many regions of the central nervous system were sampled from 10 SMA-affected and three normal Brown Swiss calves. In addition to
Vascular perfusion abnormalities in infants with spinal muscular atrophy.
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Spinal muscular atrophy (SMA) is an important cause of death in children and SMA type I, also known as Werdnig-Hoffman disease, is the most severe form of this disease. We report 2 cases of infants with SMA I in whom a distal necrosis developed, a feature not previously reported. Poor perfusion,
Cell death and decreased synaptic protein expression in the ventral horn of Holstein-Friesian calves with spinal muscular atrophy.
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A neuropathological study of Holstein-Friesian calves with spinal muscular atrophy (SMA) demonstrated decreased numbers of motor neurons in the brachial and lumbo-sacral regions of the spinal cord, together with swelling and accumulation of phosphorylated neurofilaments, and neuronophagia in most of
[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
Blood Flow to the Spleen is Altered in a Mouse Model of Spinal Muscular Atrophy.
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Spinal muscular atrophy (SMA) is a neuromuscular disorder affecting young children. While pre-clinical models of SMA show small spleens, the same is not true in humans. Here, we show by doppler ultrasonography decreased splenic blood flow in Smn2B/- mice. Further, AAV9-SMN gene therapy does not
Elevated tumor necrosis factor-alpha in skeletal muscle after stroke.
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OBJECTIVE
Tumor necrosis factor-alpha (TNF-alpha), an inflammatory cytokine negligibly expressed in normal muscle, is elevated in selected metabolic conditions characterized by muscle wasting and insulin resistance. Inflammation is fundamental to stroke pathogenesis. Stroke patients have gross
Pathogenesis of proximal autosomal recessive spinal muscular atrophy.
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Although it is known that deletions or mutations of the SMN1 gene on chromosome 5 cause decreased levels of the SMN protein in subjects with proximal autosomal recessive spinal muscular atrophy (SMA), the exact sequence of pathological events leading to selective motoneuron cell death is not fully
Motor neuron cell-nonautonomous rescue of spinal muscular atrophy phenotypes in mild and severe transgenic mouse models.
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Survival of motor neuron (SMN) deficiency causes spinal muscular atrophy (SMA), but the pathogenesis mechanisms remain elusive. Restoring SMN in motor neurons only partially rescues SMA in mouse models, although it is thought to be therapeutically essential. Here, we address the relative importance
[A cervical collar therapy for non-progressive juvenile spinal muscular atrophy of the distal upper limb (Hirayama's disease)].
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Non-progressive juvenile spinal muscular atrophy of the distal upper limb (Hirayama's disease) occurs predominantly in men in the second decade with unilateral weakness of the fingers and hand, and atrophy of the hand and forearm. The symptoms generally progress for 3-4 years after onset and then
Sustained improvement of spinal muscular atrophy mice treated with trichostatin A plus nutrition.
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Early treatment with the histone deacetylase inhibitor, trichostatin A, plus nutritional support extended median survival of spinal muscular atrophy mice by 170%. Treated mice continued to gain weight, maintained stable motor function, and retained intact neuromuscular junctions long after
A novel morpholino oligomer targeting ISS-N1 improves rescue of severe spinal muscular atrophy transgenic mice.
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In the search for the most efficacious antisense oligonucleotides (AOs) aimed at inducing SMN2 exon 7 inclusion, we systematically assessed three AOs, PMO25 (-10, -34), PMO18 (-10, -27), and PMO20 (-10, -29), complementary to the SMN2 intron 7 splicing silencer (ISS-N1). PMO25 was the most
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