Articles: human.
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J. Neuroendocrinol. · Feb 1992
Inhibition of prolactin release by gonadotropin-releasing hormone-associated Peptide in benign, dopamine-sensitive and in malignant, dopamine-resistant pituitary tumors.
Since the gonadotropin-releasing hormone-associated peptide (GAP) has been reported to be capable of inhibiting prolactin release from normal lactotrophs, with the present study we have examined the in vitro effects of GAP on prolactin release in an estrone-induced, dopamine-sensitive rat pituitary adenoma and two malignant, transplantable and dopamine-resistant rat pituitary tumors, 7315a and MtTW15. Enzymatically dispersed cells obtained from the three types of tumor were cultured in multiwell dishes for 4 days. On the fifth day, the cells were exposed for 4 h to human GAP 1-56 or to the analog GAP 42-56 or to rat GAP 1-53, at various concentrations. ⋯ Furthermore, in adenomatous cells, the inhibitory effects of these peptides were suppressed by pretreatment of the cells with pertussis toxin. These findings indicate that GAP is capable of inhibiting prolactin release even in dopamine-resistant pituitary tumors. This inhibition is exerted through a pertussis toxin-sensitive G-protein-dependent signaling mechanism in adenomatous cells.
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A series of studies with humans as well as experiments carried out on animals have shown that physical exercise leads to temporary hypoalgesia. Reduced sensitivity to pain is not only demonstrable after long-distance exercise (such as a marathon run) but also during and after intensive physical exercise on a laboratory ergometer. In a double blind study (20 mg naloxone versus placebo) experimental pain thresholds (electrical intracutaneous finger and dental pulp stimulation) and plasma hormone levels (beta-endorphin, cortisol, and catecholamines) were measured in ten healthy athletic men before, during, and after physical exercise on a cycle ergometer. ⋯ Central pain inhibitory systems are probably thereby activated by the stimulation of afferent nerves endings (group III and IV) in the skeletal muscle. The same trigger mechanism also plays a role as a release stimulus for hormones which are secreted in increased measure during physical exercise (catecholamines, pituitary hormones). Plasma beta-endorphin is probably not directly involved in the exercise-induced hypoalgesia but is rather a "marker" for the activating of central analgesia mechanisms.
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Until a short time ago, the view prevailed worldwide that children were less sensitive to pain than adults, and such operations as circumcision were performed in babies without adequate anesthesia or analgesia. This view is now considered a misconception, as psychophysiological and behavioral studies show that even neonates have a well-functioning nociceptive system. Nociception generally refers to the neural and sensory aspects of pain, which do not necessarily include conscious experience. ⋯ Thus, a considerable range of sensorimotor function, including memory, develops during fetal life. Anatomical, physiological and behavioral data suggest that the nociceptive system is included in this development. Although we cannot be sure at present whether the fetus consciously experiences pain, beyond the protective nociceptive behavioral responses, anesthesia should be used for invasive procedures to protect the fetus and its nervous systems.
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The care of severely ill patients, whether in hospital, in residential homes or in their own homes, should be characterized by humanity and dictated by efforts to make life worth living for the person concerned. Preservation of the quality of life should be paramount if the doctor can no longer effect a cure. ⋯ Close contact with members of the family and with friends and neighbours is particularly important in this phase of life. A sick person's quality of life is what the legislator had in mind when domiciliary care was given priority over residential care at the time of the legal changes to reform the health care system.
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Natl Toxicol Program Tech Rep Ser · Jun 1991
NTP Toxicology and Carcinogenesis Studies of 3,3'-Dimethylbenzidine Dihydrochloride (CAS No. 612-82-8) in F344/N Rats (Drinking Water Studies).
3,3'-Dimethylbenzidine dihydrochloride is one of five chemicals being evaluated in 2-year carcinogenicity and toxicity studies as part of the NTP's Benzidine Dye Initiative. This Initiative was designed to evaluate representative benzidine congeners, benzidine congener-derived dyes, and benzidine-derived dyes. 3,3'-Dimethylbenzidine dihydrochloride was nominated for study because of the potential for human exposure during production of bisazobiphenyl dyes and because benzidine, a structurally related chemical, is a known human carcinogen. Toxicology and carcinogenesis studies were conducted by administering 3,3'-dimethylbenzidine dihydrochloride (approximately 99% pure) in drinking water to groups of F344/N rats of each sex for 14 days, 13 weeks, or 9 or 14 months. ⋯ There was clear evidence of carcinogenic activity for female F344/N rats, as indicated by benign and malignant neoplasms of the skin, Zymbal's gland, clitoral gland, liver, oral cavity, small and large intestine, mammary gland, and lung. Increased incidences of neoplasms of the brain and mononuclear cell leukemia may have been related to chemical administration. Synonyms: o-tolidine dihydrochloride; 3,3'-dimethylbiphenyl-4,4'-diamine dihydrochloride; 3,3'-dimethylbiphenyl-4,4'-biphenyldiamine dihydrochloride; 4,4'-diamino-3,3'-dimethylbiphenyl dihydrochloride