1,721,037 research outputs found
Growth hormone-releasing hormone combined with arginine or growth hormone secretagogues for the diagnosis of growth hormone deficiency in adults.
Prolactin-releasing effect of domperidone in normoprolactinemic and hyperprolactinemic subjects
Tests of prolactin secretion in the diagnosis of hyperprolactinemic states: nomifensine and domperidone
Forty-one subjects with hyperprolactinemia underwent testing on separate occasions with nomifensine, an indirectly acting dopamine agonist, and domperidone, a dopamine receptor-blocking agent. Nomifensine (200 mg orally) did not significantly modify plasma levels of prolactin (PRL) in 17 subjects in whom the existence of a pituitary tumor had been established at surgery (12 subjects) or was highly probable (5 subjects). Of the remaining 24 patients with hyperprolactinemia of uncertain etiology, 6 had PRL responsiveness to nomifensine (decrease of baseline PRL levels greater than or equal to 30%) and 18 had PRL unresponsiveness to the drug. The administration of domperidone (4-mg bolus injected intravenously) showed in 36 of the 41 patients the existence of a homogeneity between PRL responsiveness to nomifensine and PRL responsiveness to domperidone. In only five patients was failure of nomifensine to lower plasma PRL levels associated with an increase in plasma PRL levels after domperidone administration (at least doubling of baseline PRL levels). The combined application of nomifensine and domperidone tests holds promise of being a useful method for distinguishing among hyperprolactinemic subjects those with a prolactinoma
Dynamic tests of prolactin secretion in hyperprolactinemic states: carbidopa-L-DOPA and indirectly acting dopamine agonists
Prolactin lowering effect of amphetamine in normoprolactinemic subjects and in physiological and pathological hyperprolactinemia.
The effect on plasma prolactin (PRL) of d-amphetamine (Amph) was studied in normo- and hyperprolactinemic subjects. In normoprolactinemic women Amph failed to lower plasma PRL levels when infused intravenously over 1 h at the dose of 7.5 mg, but induced at the dose of 15.0 mg a modest inhibition of plasma PRL (maximum PRL inhibition 20 +/- 4.5% at 45 min). Likewise, in puerperal women Amph at the dose of 7.5 mg did not decrease significantly plasma PRL levels but it was active in this respect (maximum inhibition 37 +/- 10% at 120 min) at the dose of 15.0 mg. In subjects with presumptive evidence of a PRL-secreting adenoma, Amph at either the 7.5 mg or the 15.0 mg dose failed to alter baseline PRL levels. These results indicate that Amph is a poor PRL suppressor in either normo- or hyperprolactinemic subjects. It is proposed that this may be due to the drug's ability to effect release of dopamine mainly from a non-granular pool of the amine
Going Beyond Counting First Authors in Author Co-citation Analysis
The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
- …
