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glutamic/atrofia

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The mechanical reliability of calcium phosphate cements has restricted their clinical application in load-bearing locations. Although their mechanical strength can be improved using a variety of strategies, their fatigue properties are still unclear, especially after degradation. The evolutions of
BACKGROUND Paraneoplastic cerebellar degeneration is a rare non-metastatic manifestation of malignancy. In this report, to the best of our knowledge we describe for the first time a diagnosis of paraneoplastic cerebellar degeneration several months prior to the diagnosis of clear carcinoma of the
Catecholaminergic innervation of luteinizing hormone-releasing hormone (LHRH) and glutamic acid decarboxylase (GAD) immunoreactive neurons in the rat medial preoptic area (MPO) was studied using electron-microscopic (EM) double-label immunostaining and combinations of single- and double-label
Kainic acid (KA)-induced degeneration of CA3 pyramidal neurons leads to synaptic reorganization and hyperexcitability in both dentate gyrus and CA1 region of the hippocampus. We hypothesize that the substrate for hippocampal inhibitory circuitry incurs significant and permanent alterations following

Apraxia in anti-glutamic acid decarboxylase-associated stiff person syndrome: link to corticobasal degeneration?

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Corticobasal syndrome (CBS) is associated with asymmetrical rigidity as well as asymmetrical limb-kinetic and ideomotor apraxia. Stiff person syndrome (SPS) is characterized by muscle stiffness and gait difficulties. Whereas patients with CBS have several forms of pathology, many patients with SPS

Spinal cord GLT-1 glutamate transporter and blood glutamic acid alterations in motor neuron degeneration (Mnd) mice.

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This study characterizes for the first time neurochemical mechanisms in Mnd mice, initially described as a model of motor neuron disease and more recently proposed as a model for neuronal ceroid lipofuscinosis. A selective decrease (-30%) of [3H]glutamate uptake was found in spinal cord but not

Cerebellar degeneration and polyglandular autoimmune syndrome with anti-glutamic acid decarboxylase antibodies.

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[The behavior of serum glutamic acid-oxalacetic acid transaminase in myopathies and neurogenic muscle atrophies].

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Glutamic-oxalacetic transaminase (GOT) in cerebrospinal fluid in patients with cerebral atrophy.

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Severe dystonia, cerebellar atrophy, and cardiomyopathy likely caused by a missense mutation in TOR1AIP1.

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BACKGROUND Dystonia, cerebellar atrophy, and cardiomyopathy constitute a rare association. METHODS We used homozygosity mapping and whole exome sequencing to determine the mutation, western blot and immunolabelling on cultured fibroblasts to demonstrate the lower expression and the mislocalization
The deep mesencephalic nucleus (DMN) is a large midbrain reticular region located between the substantia nigra compacta and the superior colliculus. It contains GABAergic cells that share striatal afferents, thalamic and collicular efferents, as well as neurochemical and electrophysiological

Development of glutamic acid decarboxylase-immunoreactive elements in the cerebellar cortex of normal and lurcher mutant mice.

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The development of glutamic acid decarboxylase-immunoreactivity (GAD-IR) in cells, fibers, and varicosities of the cerebellar cortex has been examined by light microscopy in normal and lurcher mutant mice between postnatal day 3 and 30 (P3-P30). Purkinje cell morphology was demonstrated in adjacent
Immunohistochemical expression of glutamic acid decarboxylase (GAD) enzyme was detected in the pancreatic islets of 12 cattle with spontaneous insulin-dependent diabetes mellitus (IDDM). The most characteristic changes were atrophy and decreased number of pancreatic islets, enlarged islets with
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