Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.7 (acetylcholinesterase)
 28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Paroxysmal nocturnal hemoglobinuria, first described in the late 19th century, is an acquired disorder characterized by hemoglobinemia and hemoglobinuria. The major clinical manifestation of PNH is chronic intravascular hemolysis of various severity. Patients-mostly young adults - may also present with episodes of abdominal or back pain. Common cause of death is thrombosis especially of the hepatic veins. Granulocytopenia and thrombocytopenia may be the initial manifestation of PNH, indicating that the disorder is a primary bone-marrow disease, affecting not only the erythrocytes but also other peripheral blood cells and the haematopoietic stem cell. The course of the disease is variable. Partial complete recovery was described, but also fatal thrombosis. The major phenotypic expression of PNH is an increased susceptibility of the erythrocytes to the lytic action of complement in vitro. The enhanced complement susceptibility is most probably due to membrane defects: two membrane proteins regulating the complement cascade in PNH cells were missing, the decay-accelerating factor, DAF, inhibiting the activation of the lytic complement complex and the C8 binding protein, C8bp, which interferes with the lytic process. Aside from the lack of the complement regulators also other membrane defects have been described (e.g. of acetylcholinesterase or alkaline phosphatase). The proteins as well as DAF and C8bp are linked to the cell membrane via a phosphatidylinositol (PI) anchor, leading to the speculation that the disease results from a deficiency in the post-translational PI anchoring mechanism. The diagnosis of PNH is based on the Hamtest, but will be extended to the quantitation of the above described membrane proteins.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Paroxysmal nocturnal hemoglobinuria]. 218 38

The nerves supplying the spinal dura mater were studied in four human foetuses (16-22 weeks) with the acetylcholinesterase in toto staining method. The ventral spinal dura contains a dense, longitudinally oriented, nerve plexus, which receives its contributions from: (I) the sinuvertebral nerves, (II) the nerve plexus of the posterior longitudinal ligament, (III) the nerve plexus of radicular branches of segmental arteries. Dorsal dural nerves are much smaller in number, do not form an evident plexus and do not reach the medial region of the dorsal dura. The dorsal nerves are derived from the ventral dural plexus at the level of the "intersleeval" parts of the dura mater. The ventral dural nerves may extend up to eight segments, with a great amount of overlap between adjacent nerves. This may provide an anatomical substrate for the understanding of extrasegmentally referred dural pain. The curled bundles of nerve fibres of pathways (I) and (II) provide an adequate adaptation to displacements of the spinal dura mater during flexion and extension. Pathway (III) has not been described before. The described nerve plexuses may be of importance in elucidating the mechanisms of epidural therapies in back pain and peripheral vascular disease.
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PMID:The innervation of the spinal dura mater: anatomy and clinical implications. 340 73