Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

General anaesthesia with 80% CO2/20% O2 and 5% halothane in O2 (mask induction) was compared for castration of 3-4 week-old piglets. One group was castrated without anaesthesia. Of the noncastrated control groups one had CO2- and one halothane anaesthesia, one breathed room air through the induction system, and one was held in castration position. The behaviour to induction and castration was assessed, and the cortisol-, ACTH- and beta-endorphin plasma concentrations were determined to quantify the stress elicited by anaesthesia, castration and handling. Violent struggling and vocalization were elicited by CO2 and positioning into the mask induction system while breathing room air; halothane induction was quiet. CO2 induced profound surgical anaesthesia; whereas under halothane anaesthesia some animals exhibited still a slight reaction to castration. Recovery was fast, smooth and quite. Permanent violent struggling and vocalization were elicited by castration without anaesthesia. Plasma cortisol was not a sensitive tool to judge castration stress. The high ACTH and beta-endorphin plasma concentrations elicited by CO2 anaesthesia confirm our clinical experience. General anaesthesia is fast and safely induced with CO2 in piglets and castration can be performed without any reaction, but with CO2 anaesthesia the stress is not reduced.
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PMID:Inhalation anaesthesia for the castration of piglets: CO2 compared to halothane. 992 45

Violent aggression in humans may involve a modified response to stress, but the underlying mechanisms are not well understood. Here we show that naturally present autoantibodies reactive to adrenocorticotropic hormone (ACTH) exhibit distinct epitope-binding profiles to ACTH peptide in subjects with a history of violent aggression compared with controls. Namely, while nonaggressive male controls displayed a preferential IgG binding to the ACTH central part (amino acids 11-24), subjects who had committed violent acts of aggression had IgG with increased affinity to ACTH, preferentially binding to its N terminus (amino acids 1-13). Purified IgGs from approximately half of the examined sera were able to block ACTH-induced cortisol secretion of human adrenal cells in vitro, irrespective of the source of sample (from a control subject or a violent aggressor). Nevertheless, in the resident-intruder test in mice, i.p. injection of residents with ACTH and IgG from aggressive subjects, but not from control subjects, shortened latency for the first attack against intruders. Immunohistochemical screening of violent aggressors' sera on rat brain and pituitary sections did not show IgG binding to ACTH-producing cells, but 4 of 16 sera revealed selective binding to a nonidentified antigen in vasopressinergic neurons of the hypothalamic paraventricular and supraoptic nuclei. Thus, the data show that ACTH-reactive plasmatic IgGs exhibit differential epitope preference in control and violently aggressive subjects. These IgGs can modulate ACTH-induced cortisol secretion and, hence, are involved in the regulation of the stress response. However, the possible role of ACTH-reactive autoantibodies in aggressive behavior needs further investigation.
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PMID:Autoantibodies reactive to adrenocorticotropic hormone can alter cortisol secretion in both aggressive and nonaggressive humans. 2994 62