Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0262471 (ENT)
 5,307 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Norethindrone (ENT), which is a representative in estrane series of progestogen, is not only strongly progestational but also estrogenic and in some cases, antiestrogenic. To understand progestational effect and antiestrogenic effect, the interactions of ENT on estrogen and progestogen receptors were studied in the uterine cytosol of white female rabbit. The 274,200 X G supernatant of uterine homogenate was used as cytosol. 3H-Estradiol, 3H-Progesterone, 3H-ENT or cold ENT were incubated with uterine cytosol at 4 degrees C for 2 hours. Results are as follows: 1. Sucrose gradient centrifugation [5 approximately 20% linear and 40,000 rpm (159,200 X G) for 16 hours at 4 degrees C]: ENT was bound to extrogen 8S receptor in immature rabbit uterus (Fig. 2 & 3), and to progestogen 8S receptor in estrogen primed rabbit uterus (Fig. 5). 2. Kinetic study, determined by dextran coated charcoal (0.001% dextran and 0.1% charcoal): (1) In the uterine cytosol of immature rabbit, 3H-estradiol-receptor binding was observed with Kd divide by 3.6 X 10-9 M and it was revealed that ENT was a competitive inhibitor to this binding with Ki divide by 2.6 X 10-6 M, as in Fig. 6. (2) 8S component, obtained by centrifugation of uterine cytosol (Fig. 1) in estrogen primed rabbit, binds 3H-progesterone with Kd divide by 8.1 X 10-10 M and Bm (maximal binding sites) divide by 5.0 X 10-8 M/mg of protein, and ENT was a competitive inhibitor in this binding with Ki divide by 2.3 X 10-9 M (FIG. 7 & 8). 3H-ENT-8S binding was demonstrated with Kd divide by 1.1 X 10-9 M and Bm divide by 8.7 X 10-8 M/mg of cytosol protein (Fig. 8). These results indicate: (a) ENT is bound to both estrogen and progestogen receptors in 8S macromolecules of uterine cytosol, (b) competitive inhibition of ENT to these bindings indicated that ENT is bound to these receptors at the steroid binding sites where estradiol and progesterone bind to, (c) ENT has much more affinity to progestogen receptor (Ki divide by 2.3 X 10-9 M) than to estrogen receptor (Ki divide 2.6 X 10-6 M), (d) while ENT is bound to progestogen and estrogen receptors at the same time, Bm of ENT (8.7 X 10-8 M/mg of cytosol protein) is more than Bm of progesterone (5.0 X 10-9 M/mg of cytosol protein), and Kd of ENT (1.1 X 10-9 M) was less than Ki of ENT (2.3 X 10-9 M) in the binding to progesterone-receptor. Biologically, while ENT is bound to progestogen -receptor with high affinity and to estrogen receptor with low affinity, ENT is actually progestational in low dose and antiestrogenic in high dose but the anti-estrogenicity seems to be incomplete in vivo as ENT may be metabolized to a potent estrogenic compound, ethinyl estradiol
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PMID:[Interaction of norethindrone on estrogen and progesterone receptors in the rabbit uterine cytosol (author's transl)]. 18 90

The effects of P and six synthetic steroids (MPA, ENT, CAP, R2323, DL and EEL) on estradiol dehydrogenase (E2DH) activity were studied in normal human uterine endometrium in vitro. The mean value of E2DH activity in the proliferative endometrium was 1.5 +/- 0.2 nmol/mg protein/h and that in the secretory endometrium was 10.2 +/- 1.1 nmol/mg protein/h. There was a 7-fold increase in the secretory phase. E2DH activity in the uterine endometrium was stable during the culture period of up to 72 h. In the proliferative endometrium, P, MPA and ENT (approximately 10(-6)M) induced E2DH activity during a 24-h incubation. CAP and R2323 had no significant effect. EEL and DL had negligible effects. In contrast, E2DH activity in the secretory endometrium was not induced further by the steroids. Therefore, in the proliferative endometrium, the elevation of E2DH activity is attributable to the progestational activity and, in the secretory endometrium, E2DH activity is not increased further by the progestational agents because it has been already activated fully by P.
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PMID:Induction of estradiol dehydrogenase activity in human uterine endometrium by synthetic steroids. 246 May 16

In this study, the Cochlear Implant Programme of the ENT Department of Ospedale Civile di Venezia, is presented. Between 1989 and 1994, after a rigorous selection process, 36 patients were selected to be implanted with a cochlear prostheses: 28 with the multichannel Nucleus 22 device, 5 with the Clarion implant and 3 with the single channel Med-E1 BTE device. The distribution of the patients according to age, etiology, duration of auditory deprivation, age at onset of deafness, is presented. The different speech-coding strategies of the Nucleus system (Wearable Speech Processing, Multipeak speech processing and Spectral Maximum Sound processor) and the stimulation mode (common ground, bipolar, bipolar + 1) as well as the Clarion speech coding strategy (Continuous Interleaved Samples and Compressed Analog) are briefly discussed. The rehabilitation programme, the specific speech recognition assessment test batteries-Consonant Confusion Test, Vocal Confusion Test, Speech Tracking, MAC battery-as they are employed in our department, are presented. As we have analyzed our results, certain factors appear as predicting a favourable outcome: - age of onset of deafness; postlingual patients, who have developed communication skills compare favourably to the perilingual group. - durations of auditory deprivation, as it is related to surviving cells in the cochlea: the shorter the period of deafness, the better the results. - length of electrode insertion, as it is determined by ossification of the cochlea. - high dynamic range of the MAP. - percent of activated electrodes: a number of 10 active electrodes or less predicts a poor outcome. - for simplification reasons, a new variable is introduced-Auditory Deprivation Index- and its positive correlation to the performance presented. - the time period of experience with the device, length and quality of rehabilitation and family support have to be mentioned.
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PMID:[Considerations on the rehabilitation of the hearing in cochlear implant patients]. 908 26