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Neuroleptic Malignant Syndrome
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D009459 |
[A potentially fatal syndrome associated primarily with the use of neuroleptic agents (see ANTIPSYCHOTIC AGENTS) which are in turn associated with dopaminergic receptor blockade (see RECEPTORS, DOPAMINE) in the BASAL GANGLIA and HYPOTHALAMUS, and sympathetic dysregulation. Clinical features include diffuse MUSCLE RIGIDITY; TREMOR; high FEVER; diaphoresis; labile blood pressure; cognitive dysfunction; and autonomic disturbances. Serum CPK level elevation and a leukocytosis may also be present. (From Adams et al., Principles of Neurology, 6th ed, p1199; Psychiatr Serv 1998 Sep;49(9):1163-72)
] |
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Neurofibromatosis 1
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D009456 |
[A syndrome characterized by the presence of PULMONARY STENOSIS; CAFE-AU-LAIT SPOTS; MENTAL RETARDATION; and short stature caused by mutations in the NF1 gene (GENES, NEUROFIBROMATOSIS 1).
, An autosomal dominant inherited disorder (with a high frequency of spontaneous mutations) that features developmental changes in the nervous system, muscles, bones, and skin, most notably in tissue derived from the embryonic NEURAL CREST. Multiple hyperpigmented skin lesions and subcutaneous tumors are the hallmark of this disease. Peripheral and central nervous system neoplasms occur frequently, especially OPTIC NERVE GLIOMA and NEUROFIBROSARCOMA. NF1 is caused by mutations which inactivate the NF1 gene (GENES, NEUROFIBROMATOSIS 1) on chromosome 17q. The incidence of learning disabilities is also elevated in this condition. (From Adams et al., Principles of Neurology, 6th ed, pp1014-18) There is overlap of clinical features with NOONAN SYNDROME in a syndrome called neurofibromatosis-Noonan syndrome. Both the PTPN11 and NF1 gene products are involved in the SIGNAL TRANSDUCTION pathway of Ras (RAS PROTEINS).
] |
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Myosin Type III
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D08.811.913.696.310 |
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Sleep, Slow-Wave
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F02.830.855.796.835 |
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Neuroglia
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D009457 |
[The non-neuronal cells of the nervous system. They not only provide physical support, but also respond to injury, regulate the ionic and chemical composition of the extracellular milieu, participate in the BLOOD-BRAIN BARRIER and BLOOD-RETINAL BARRIER, form the myelin insulation of nervous pathways, guide neuronal migration during development, and exchange metabolites with neurons. Neuroglia have high-affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitters, but their role in signaling (as in many other functions) is unclear.
] |
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Peptide Chain Termination, Translational
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D010443 |
[A process of GENETIC TRANSLATION whereby the terminal amino acid is added to a lengthening polypeptide. This termination process is signaled from the MESSENGER RNA, by one of three termination codons (CODON, TERMINATOR) that immediately follows the last amino acid-specifying CODON.
] |
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Neuromuscular Agents
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D009465 |
[Drugs used for their actions on skeletal muscle. Included are agents that act directly on skeletal muscle, those that alter neuromuscular transmission (NEUROMUSCULAR BLOCKING AGENTS), and drugs that act centrally as skeletal muscle relaxants (MUSCLE RELAXANTS, CENTRAL). Drugs used in the treatment of movement disorders are ANTI-DYSKINESIA AGENTS.
] |
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Peptide Elongation Factor Tu
|
D010444 |
[A protein found in bacteria and eukaryotic mitochondria which delivers aminoacyl-tRNA's to the A site of the ribosome. The aminoacyl-tRNA is first bound to a complex of elongation factor Tu containing a molecule of bound GTP. The resulting complex is then bound to the 70S initiation complex. Simultaneously the GTP is hydrolyzed and a Tu-GDP complex is released from the 70S ribosome. The Tu-GTP complex is regenerated from the Tu-GDP complex by the Ts elongation factor and GTP.
] |
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Neuromuscular Blocking Agents
|
D009466 |
[Drugs that interrupt transmission of nerve impulses at the skeletal neuromuscular junction. They can be of two types, competitive, stabilizing blockers (NEUROMUSCULAR NONDEPOLARIZING AGENTS) or noncompetitive, depolarizing agents (NEUROMUSCULAR DEPOLARIZING AGENTS). Both prevent acetylcholine from triggering the muscle contraction and they are used as anesthesia adjuvants, as relaxants during electroshock, in convulsive states, etc.
] |
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Treponema Immobilization Test
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E05.200.812.735.850.800 |
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Peptide Elongation Factors
|
D010445 |
[Protein factors uniquely required during the elongation phase of protein synthesis.
] |
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Trichostrongyloidiasis
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C01.610.335.508.700.775.825 |
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Megacolon, Toxic
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C06.405.469.158.701.591 |
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Neuroma
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D009463 |
[A tumor made up of nerve cells and nerve fibers. (Dorland, 27th ed)
] |
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Peptide Fragments
|
D010446 |
[Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.
] |
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Neuroma, Acoustic
|
D009464 |
[A benign SCHWANNOMA of the eighth cranial nerve (VESTIBULOCOCHLEAR NERVE), mostly arising from the vestibular branch (VESTIBULAR NERVE) during the fifth or sixth decade of life. Clinical manifestations include HEARING LOSS; HEADACHE; VERTIGO; TINNITUS; and FACIAL PAIN. Bilateral acoustic neuromas are associated with NEUROFIBROMATOSIS 2. (From Adams et al., Principles of Neurology, 6th ed, p673)
] |
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Peptide Hydrolases
|
D010447 |
[Hydrolases that specifically cleave the peptide bonds found in PROTEINS and PEPTIDES. Examples of sub-subclasses for this group include EXOPEPTIDASES and ENDOPEPTIDASES.
] |
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Neurologic Manifestations
|
D009461 |
[Clinical signs and symptoms caused by nervous system injury or dysfunction.
] |
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Peptide Initiation Factors
|
D010448 |
[Protein factors uniquely required during the initiation phase of protein synthesis in GENETIC TRANSLATION.
] |
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Neurology
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D009462 |
[A medical specialty concerned with the study of the structures, functions, and diseases of the nervous system.
] |
