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11,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The potential effect of intracerebroventricular (icv) alpha N-acetyl human beta-endorphin-(1-31) on morphine dependence was examined in mice and rats. Animals were rendered tolerant-dependent by subcutaneous (sc) implantation of an oily suspension (10 ml/Kg mouse and 3 ml/Kg rat) containing 0.1 g/ml of morphine. After 72 h of chronic morphine, 1 mg/Kg sc naloxone precipitated in both species a withdrawal syndrome that was moderate in animals pretreated with the acetylated derivative of beta-endorphin. Doses of 28 fmols/rat or 80 fmols/mouse alpha N-acetyl human beta-endorphin-(1-31) reduced the number of animals presenting the jumping behaviour, as well as the number of jumps recorded. Moreover, less than half of the rats presented the other withdrawal signs evaluated: squeak on touch, diarrhoea, chattering, chewing, ptosis and body shakes. This activity could be observed when alpha N-acetyl human beta-endorphin was injected 1 h to 24 h before naloxone; longer intervals resulted in a significant loss of this activity. The alpha 2 agonist clonidine given icv at pmol-nmol doses decreased the incidence of morphine withdrawal syndrome. Combinations of these two substances generally did not produce any further enhancement of the effects of clonidine and alpha N-acetyl beta-endorphin when used alone. Icv injections of the antagonist of alpha 2-adrenoceptors yohimbine prevented both clonidine and alpha N-acetyl beta-endorphin-(1-31) from reducing the jumping behaviour displayed by morphine-abstinent mice. It is suggested that alpha N-acetyl beta-endorphin produces this alleviation of the morphine withdrawal syndrome by improving the efficiency of alpha 2-mediated agonist effects after acting on a neural substrate that is distinct from the mu opioid receptor binding site.
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PMID:alpha N-acetyl human beta-endorphin-(1-31) alleviates the morphine withdrawal syndrome in rodents: a comparative study with clonidine. 160 92

The purpose of this study was to evaluate and compare thin-section magnetic resonance imaging (MRI) and high-resolution computed tomography (CT) in patients with suspected pituitary adenomas. Twenty-two patients (19 women and three men) with hyperprolactinemia (N = 16), increased growth hormone secretion (N = 2), increased corticotropin secretion (N = 1), and nonsecreting adenomas (N = 3) were studied with both contrast-enhanced, high-resolution CT scanning and thin-section MRI. Contrast-enhanced examinations consisted of contiguous 1.5-mm coronal sections during contrast infusion. The MRI examinations consisted of spin-echo T1- and T2-weighted sequences with a 2.5-3.0-mm slice thickness on the coronal and sagittal planes. Fourteen women had similar findings on CT and MRI (four macroadenomas, six microadenomas, one wide stalk, two empty sellas, and one normal study). The remaining eight subjects had conflicting results: CT findings were compatible with a microadenoma in all eight patients, whereas MRI detected one enlarged pituitary, two empty sellas (one with prolapse of the optic chiasm) without evidence of adenoma, and five normal examinations. Thus, both studies detected macroadenomas accurately, but CT was frequently unable to diagnose correctly an empty sella. Because patients with possible microadenomas were not submitted to surgery, the accuracy of either radiologic method cannot be assessed at this time. However, we suggest that MRI is superior to CT because of its inherently greater soft-tissue contrast, which allows clear visualization of the optic chiasm, optic nerves, cavernous sinuses, and carotid arteries.
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PMID:Computed tomography versus magnetic resonance imaging for the evaluation of suspected pituitary adenomas. 272 20

The effects of CRF, ACTH 1-24, alpha-MSH, and an ACTH 4-49 analog, at doses of 0, 0.1, 1, and 10 mg/kg, were tested on temperature, ptosis, and sedation in mice pretreated 18 hr previously with reserpine. IP injection of CRF at doses of 1 and 10 mg/kg significantly potentiated the reserpine-induced hypothermia while ACTH 1-24 at the same two doses had the opposite effect of significantly reversing the hypothermia as compared to diluent. The highest dose of alpha-MSH exerted a similar action to that of ACTH 1-24, but none of the doses of the ACTH 4-9 analog changed body temperature. beta-endorphin also failed to cause a reliable effect even though naloxone blocked the action of CRF on body temperature. The results suggest that CRF, like other hypothalamic peptides, can exert extra-pituitary actions after peripheral administration.
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PMID:Opposite effects of CRF and ACTH on reserpine-induced hypothermia. 629 33

Chronic morphine exposure induces physical dependence and tolerance. Previous studies have shown that there is a decrease in met-enkephalin levels in states of morphine physical dependence, and that increasing enkephalin during opiate physical withdrawal ameliorates the severity of the morphine withdrawal syndrome. In order to investigate the role of spinal opioid peptide in the phenomenon of naloxone-precipitated withdrawal we examined the effect of herpes simplex virus vector-mediated overexpression of proenkephalin in lumbar dorsal root ganglia in rats with neuropathic pain treated with morphine. The morphine physical dependence was induced by chronic administration of intraperitoneal (IP) morphine for 2 weeks. Rats with neuropathic pain inoculated subcutaneously with the vector-mediated overexpression of proenkephalin showed a significant reduction in jumps, 'wet-dog' shakes, diarrhea and ptosis precipitated by naloxone after 2 weeks of morphine treatment. The global withdrawal score was also reduced significantly by vector-mediated overexpression of proenkephalin. These studies demonstrate a role for opioid peptide in the spinal cord in mediating some of the withdrawal response.
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PMID:Transgene-mediated enkephalin expression attenuates signs of naloxone-precipitated morphine withdrawal in rats with neuropathic pain. 1876 80

The use of navigation systems is safe and reliable for neurological surgery. We performed endoscopic transsphenoidal surgery to totally resect an adrenocorticotropic hormone (ACTH)-producing pituitary adenoma associated with oculomotor nerve palsy. A 70-year-old woman developed right ptosis 4 months before admission. She developed anisocoria 2 months later and was referred to the department of neurology from clinic. Brain magnetic resonance imaging(MRI)showed an intrasellar tumor that partially invaded the right cavernous sinus, and she was then referred to our department. She exhibited a round face ("moon face") and central obesity. Laboratory test results showed a high urinary cortisol level and high serum ACTH level, and neither the serum cortisol nor ACTH level was suppressed by a low-dose dexamethasone test. We performed transsphenoidal surgery using high-dimensional endoscopy under electromagnetic navigation. The tumor invading the cavernous sinus was visualized via endoscopy and confirmed on navigation using a flexible needle probe. Postoperative MRI showed total removal of the tumor, and the serum ACTH level recovered to the normal range. The patient's right oculomotor palsy resolved within 1 week postoperatively. In summary, electromagnetic navigation was useful for total resection of a pituitary tumor invading the cavernous sinus, contributing to normalization of the ACTH level and improvement in neurological symptoms.
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PMID:[A Case of an Adrenocorticotropic Hormone-Producing Pituitary Adenoma Removed via Electromagnetic-Guided Neuroendoscopy]. 2727 Jan 45