Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1519176 (PSA)
 5,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The seminal vesicles originate in embryos of about 58 mm crown-rump-length from the Wolffian duct under the influence of testosterone. Along with the ampulla of the vas deferens and the ejaculatory duct, they form a functional unit that develops slowly until the onset of puberty. Developmental malformations occur as uni- or bilateral agenesis, aplasia, cysts, or ureterovesicular fistules. After puberty, the glands form sac-like structures which have a capacity of about 3.4-4.5 ccm and contribute about 70% of the seminal fluid. In addition to secretion, they are capable of reabsorption of fluids or dissolved substances, and of spermatophagy (ingestion and degradation of damaged spermatozoa by epithelial cells). Secretory activity of the glands is a measure of testosterone supplementation to the epithelium. Nervous regulation of secretion is realized by cholinergic post-ganglionic, sympathetic (and perhaps parasympathetic) fibres, derived from pelvic plexus. Contraction of the muscular wall occurs under the influence of excitatory adrenergic and modulatory NPY-encephalin-peptidergic nerve fibres. The secretory products of the seminal vesicles encompass (1) ions (K+: 1.1 mM ml-1) (2) low molecular weight substances (fructose: above 1.2 mg ml-1; prostaglandins above 250 microliters ml-1, (3) peptides (endorphin: 330 pg ml-1), and (4) proteins. In addition to plasma protein related forms such as transferrin, lactoferrin, and fibronectin, specific proteins such as semenogelin (52 kDa) are synthesized, the scaffold protein of semen coagulate forming the substrate for PSA (prostate specific antigen), sperm motility inhibitor (ca. 18 kDa), and others (placental protein 5, protein kinase inhibitor, carboanhydrase, 5'-nucleotidase), some of which are immunosuppressive. Therefore, functions of the seminal vesicles concern (a) formation of seminal coagulum, (b) modification of sperm functions (motility, capacitation), and (c) immunosuppression. Additional functions within the female genital system, perhaps during pre-implantation period, are likely, but remain to be proven experimentally.
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PMID:Morphology and functions of the human seminal vesicle. 164 33

Chronic immobilization stress (CIS) shortens apical dendritic trees of CA3 pyramidal neurons in the hippocampus of the male rat, and dendritic length may be a determinant of vulnerability to stress. Expression of the polysialylated form of neural cell adhesion molecule (PSA-NCAM) in the hippocampal formation is increased by stress, while PSA removal by Endo-neuraminidase-N (endo-N) is known to cause the mossy fibers to defasciculate and synapse ectopically in their CA3 target area. We show here that enzymatic removal of PSA produced a remarkable expansion of dendritic arbors of CA3 pyramidal neurons, with a lesser effect in CA1. This expansion eclipsed the CIS-induced shortening of CA3 dendrites, with the expanded dendrites of both no-stress-endo-N and CIS-endo-N rats being longer than those in no-stress-control rats and much longer than those in CIS-control rats. As predicted by the hypothesis that endo-N-induced dendritic expansion might increase vulnerability to excitotoxic challenge, systemic injection with kainic acid, showed markedly increased neuronal degeneration, as assessed by fluorojade B histochemistry, in rats that had been treated with endo-N compared to vehicle-treated rats throughout the entire hippocampal formation. PSA removal also exacerbated the CIS-induced reduction in body weight and abolished effects of CIS on NPY and NR2B mRNA levels. These findings support the hypothesis that CA3 arbor plasticity plays a protective role during prolonged stress and clarify the role of PSA-NCAM in stress-induced dendritic plasticity.
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PMID:Depletion of polysialic acid from neural cell adhesion molecule (PSA-NCAM) increases CA3 dendritic arborization and increases vulnerability to excitotoxicity. 2321 84