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1 LHRH agonists provide an additional class of agents for
2 LHRH agonists showed similar efficacy to chemotherapy (r
3 LHRH agonists were ineffective in hormone-receptor-negat
4 LHRH cell number after drug treatment as determined by i
5 LHRH cells exhibit neurophilic migration moving from the
6 LHRH mRNA levels were examined in young and middle-aged
7 LHRH mRNA levels were measured in cytosolic extracts, an
8 LHRH patients assessed their overall health as fair or p
9 LHRH patients reported more breast swelling than did orc
10 LHRH patients reported more physical discomfort and worr
11 LHRH receptors are expressed in a very high percentage o
12 LHRH-conjugated nanocapsules selectively delivered recom
13 LHRH-negative neurons in culture exhibited only occasion
14 LHRH-R mRNA expression in female pituitaries was reduced
16 e not known to self-aggregate (amylin, ACTH, LHRH, angiotensin II, atrial natriuretic peptide, somato
17 e c-Fos expression in both SCN and activated LHRH neurons, with the percentage of LHRH+/c-Fos+ double
21 onal pseudorabies virus into the brain of an LHRH::CRE mouse line led to the identification of neuron
24 trial to determine whether treatment with an LHRH agonist increases adult height in short adolescents
27 d, the subjects who had been treated with an LHRH agonist were older than those who had received plac
29 nd diminished LHRH-R mRNA to 30% and 26% and LHRH-R protein to 57% and 48% on days 10 and 30, respect
31 lly, we showed that Mn2+ stimulated cGMP and LHRH from the same tissues, and that downstream blocking
32 els were measured in cytosolic extracts, and LHRH primary transcript levels were measured in nuclear
34 suppress pituitary gonadotroph functions and LHRH-receptor (LHRH-R) expression are incompletely under
35 Preclinical studies revealed that GHRH and LHRH antagonists both can cause a reduction in prostate
40 vealed dual expression of nestin protein and LHRH in cells proximal to the vomeronasal organ anlage t
42 in Locke solution for 30 min to assess basal LHRH secretion, then incubated with buffer alone or buff
43 gonadotropin release in the presence of both LHRH and AA, whereas sodium nitroprusside, a releaser of
44 bypassed the surge in sex steroids caused by LHRH agonists, the gold standard for clinical ablation o
48 (LHRH) release, we examined whether cultured LHRH neurons exhibit spontaneous intracellular Ca(2+) ([
50 was performed to compare the 3-monthly depot LHRH agonist leuprorelin acetate (LAD-3M; n = 299) and c
53 duced serum LH in female rats and diminished LHRH-R mRNA to 30% and 26% and LHRH-R protein to 57% and
55 ng 100 microg of peptide daily, the elevated LHRH-R mRNA level was decreased by 73%, whereas daily in
57 heterozygous deletion in the nasal embryonic LHRH factor (NELF) gene in pedigree 1 and an additional
58 ion of a novel factor termed nasal embryonic LHRH factor (NELF) that was discovered in a differential
64 and its ability to counteract the exogenous LHRH and the agonist triptorelin in the regulation of th
69 onic stage before the migration of bona fide LHRH neurons, and is ultimately distributed in the extra
75 which is similar to the period observed for LHRH release, whereas in 5 of 17 cultures the less tight
76 tors, receptor protein and binding sites for LHRH were detected in both transplantable melanoma tumor
79 es of luteinizing hormone-releasing hormone (LHRH) -like neurons, "early" and "late" cells, were disc
80 f the luteinizing hormone-releasing hormone (LHRH) agonist Decapeptyl (25 microg/day) for 30 days or
81 ith a luteinizing hormone-releasing hormone (LHRH) agonist increases adult height in children with LH
83 with luteinizing hormone-releasing hormone (LHRH) agonists is an effective adjuvant treatment for pr
84 with luteinising-hormone-releasing hormone (LHRH) agonists, but results have been inconclusive, espe
87 luteinizing hormone (LH)-releasing hormone (LHRH) antagonists suppress pituitary gonadotroph functio
88 og of luteinizing hormone-releasing hormone (LHRH) as a targeting moiety specific to the receptors th
90 o the luteinizing hormone-releasing hormone (LHRH) neuroendocrine phenotype are derived from the nasa
94 population afferent to LH-releasing hormone (LHRH) neurons that is co-activated to express c-Fos with
95 lates luteinizing hormone releasing hormone (LHRH) neurons to secrete LHRH, the neuropeptide controll
97 ct of luteinizing hormone-releasing hormone (LHRH) on luteinizing hormone secretion in several specie
98 with luteinizing hormone-releasing hormone (LHRH) peptide via phospholipid, the fcc-FePt NPs can bin
99 ) and luteinizing hormone releasing hormone (LHRH) peptide, resulting in specific and efficient accum
100 ed by luteinizing hormone-releasing hormone (LHRH) receptor antagonism bypassed the surge in sex ster
101 ly inhibits stimulated LH-releasing hormone (LHRH) release from medial basal hypothalamic explants.
102 atile luteinizing hormone-releasing hormone (LHRH) release, we examined whether cultured LHRH neurons
103 ts of luteinizing hormone-releasing hormone (LHRH) release, which was monitored as slow membrane depo
104 ol of luteinizing hormone-releasing hormone (LHRH) secretion and sexual behavior which show diurnal v
108 ue of luteinizing hormone releasing hormone (LHRH), AN-207, binds with high affinity to LHRH receptor
109 on of luteinizing hormone releasing hormone (LHRH), growth hormone releasing hexapeptide (GHRP-6), an
110 st of luteinizing hormone-releasing hormone (LHRH), reduces levels of serum LH, estradiol, progestero
111 on of luteinizing hormone-releasing hormone (LHRH), the neuropeptide controlling sexual development,
112 on of luteinizing hormone-releasing hormone (LHRH), the neuropeptide controlling sexual development.
116 wn as luteinizing hormone releasing hormone (LHRH)] neurons can exhibit synchronized neuroendocrine s
117 izing luteinizing hormone-releasing hormone (LHRH, also known as gonadotropin-releasing hormone [GnRH
119 sion (luteinizing hormone-releasing hormone [LHRH] agonist), whereas 75 patients received radiation a
121 4 has 1-2 nM affinity for both rat and human LHRH receptors and is a potent inhibitor of LH release (
122 t findings suggest that the hypophysiotropic LHRH-synthesizing neurons may be innervated by intrahypo
123 ctively, for patients who received immediate LHRH agonist versus 10% [corrected] and 4% for patients
125 upport a role for age-related alterations in LHRH gene expression in the disruption of regular estrou
129 onsistent with a role for dynamic changes in LHRH transcriptional activity in modulating parameters o
136 een postulated that the pubertal increase in LHRH secretion in female animals also requires neuron-gl
139 es of evidence that PSA-NCAM plays a role in LHRH cell migration: promotion of cell movement along th
141 dings suggest a potential role for increased LHRH gene transcription in the accumulation of LHRH prio
142 nicotine at very low concentrations induced LHRH release via a Na+-dependent, Ca2+-independent mecha
144 and reversibly blocked the nicotine-induced LHRH release, but it did not block the nerve-firing-evok
145 d 250 microM MnCl2 all significantly induced LHRH release, the two lowest doses did not stimulate tot
147 iption-PCR analyses were used to investigate LHRH receptors in MRI-H255 and MRI-H187 transplantable h
150 tantly, neurons that expressed l-GnRH-III, m-LHRH, or both peptides were also detected in the ventral
151 Immunopositive neurons for l-GnRH-III, m-LHRH, or neurons coexpressing both peptides were detecte
155 mone release but also are colocalized with m-LHRH neurons in areas primarily controlling LH release.
156 tes, a group of neurons containing mammalian LHRH mRNA arises at an early embryonic stage before the
160 s are found in the basal forebrain, and many LHRH neurons are displaced into the cerebral cortex of D
163 M, and a preference of a subset of migrating LHRH cells for a PSA-positive axon branch over a PSA-neg
166 sary for establishment of the neuroendocrine LHRH system, cells critical for reproductive function.
168 data indicate that, in primary LHRH neurons, LHRH mRNA has an intrinsically high rate of turnover and
169 itary cells in vitro to 3-min pulses of 1 nM LHRH or 0.1 nM triptorelin for 5 h increased the LHRH-R
172 RH gene transcription in the accumulation of LHRH prior to the start of the LH surge and in the reple
176 neuraminidase N, followed by the analysis of LHRH cell positions, and examination of LHRH cell positi
177 the direct inhibitory action of GHRH and of LHRH antagonists exerted through prostatic receptors.
179 en both AA and an effective concentration of LHRH were incubated together, there was no additive resp
180 n sites, the distribution and connections of LHRH and NPY-immunoreactive (IR) neuronal elements in th
182 eatment time showed a rapid initial decay of LHRH mRNA (t1/2, 5-13 min), followed by a slower decay r
187 uently, we investigated the direct effect of LHRH antagonist cetrorelix in vitro on the expression of
190 s of LHRH cell positions, and examination of LHRH cell positions in mutant mice deficient in the expr
191 Blockade of LHRH receptors by an excess of LHRH agonist Decapeptyl suppressed the effects of AN-207
193 one inhibition is manifested by a failure of LHRH and pePOA neurons to become activated at the time o
195 study, we investigated the molecular form of LHRH in the "early" cells in the nasal regions and brain
199 t effect observed was dramatic inhibition of LHRH cell migration in explants cultured in the presence
203 ns can have profound effects on migration of LHRH neurons and suggests that GABA participates in appr
204 t outgrowth of olfactory axons, migration of LHRH neurons in association with a subset of these axons
206 Accordingly, chemosensory modulation of LHRH neuronal activity and mating behavior are dramatica
207 rast to established notions on the nature of LHRH neuronal inputs, our data identify major olfactory
208 migration, resulting in an excess number of LHRH cells in the accessory olfactory bulb, was observed
211 placode and the ventral migratory pathway of LHRH neurons from rhesus monkey embryos at embryonic age
212 tivated LHRH neurons, with the percentage of LHRH+/c-Fos+ double-labeled cells approximately fivefold
214 tectable response of the cytoplasmic pool of LHRH mRNA to changes in gene transcription at this time.
218 one secretion, caused by impaired release of LHRH, the hypothalamic neuropeptide that controls sexual
220 ODQ blocked the Mn2+-stimulated secretion of LHRH in a dose-dependent manner, indicating that GC is t
221 rnating left- and right-sided stimulation of LHRH neurons; under such circumstances, the functional a
229 we evaluated the role of GABAergic input on LHRH neuronal migration using olfactory explants, previo
230 the effect of GABAA receptor stimulation on LHRH and/or gonadotropin release in prepubertal animals,
232 in the vomeronasal organ anlage that turn on LHRH gene and peptide expression subsequently migrate in
234 st Decapeptyl (25 microg/day) for 30 days or LHRH antagonist Cetrorelix pamoate (100 microg/day) for
236 e of gonadotropin-releasing hormone (GnRH or LHRH), is the active pharmaceutical ingredient used to t
237 dotropin hormone releasing hormone (GnRH, or LHRH) neurons in the rostral medial preoptic region of t
238 cancer cell line (A2780) that overexpresses LHRH receptors and exhibit high toxicity to these tumor
240 rum LH and testosterone levels and pituitary LHRH-R in male rats are also decreased by high doses of
241 days on the expression of mRNA for pituitary LHRH receptor (LHRH-R) and the levels of LHRH-R protein
242 effect of Cetrorelix on serum LH, pituitary LHRH-R mRNA, and LHRH-R protein was greater than that of
243 esterone, and the concentration of pituitary LHRH receptors (LHRH-Rs) and their mRNA expression.
244 ix, inhibit the gene expression of pituitary LHRH-R indirectly, by counteracting the stimulatory effe
245 in vitro on the expression of the pituitary LHRH-R gene and its ability to counteract the exogenous
246 ined LHRH mRNA turnover in primary postnatal LHRH neurons maintained in long-term hypothalamic/preopt
248 roscopy revealed that subsets of prepubertal LHRH neurons are endowed with alpha 1, alpha 2, beta 2/3
251 cotinic acetylcholine receptors and produced LHRH release via a mechanism that is different from the
252 f LH responses in female rats, while raising LHRH-R mRNA expression in female rats by 23% and LHRH-R
253 ression of mRNA for pituitary LHRH receptor (LHRH-R) and the levels of LHRH-R protein were evaluated
257 l cell type of the median eminence, regulate LHRH release during the estrous cycle by undergoing plas
259 releasing hormone (LHRH) neurons to secrete LHRH, the neuropeptide controlling sexual development.
265 al studies in rodents have demonstrated that LHRH neurons are innervated by GABA-containing processes
269 y GABA-containing processes, suggesting that LHRH secretion is under direct transsynaptic GABAergic c
272 of difference in overall survival among the LHRH agonists, although CIs were wider for leuprolide (h
274 tion of treatment was 3.5+/-0.9 years in the LHRH-agonist group and 2.1+/-1.2 years in the placebo gr
278 nhibited the migration of nearly half of the LHRH neuron population, without affecting the VNN tract
279 tration of cetrorelix and triptorelin on the LHRH-R mRNA level and gonadotropin secretion in ovariect
280 le rats, cetrorelix treatment suppressed the LHRH-R mRNA level by 33%, but triptorelin increased it b
281 ructural analysis would demonstrate that the LHRH system in the human hypothalamus is regulated by NP
282 viewed in relation to circulating LH titers, LHRH primary transcript levels were high prior to the st
284 (LHRH), AN-207, binds with high affinity to LHRH receptors and can be targeted to tumors expressing
288 ) was used as a targeting moiety (ligand) to LHRH receptors that are overexpressed in the plasma memb
289 together, there was no additive response to LHRH and the response was the same as to either compound
290 sed as the only systemic adjuvant treatment, LHRH agonists did not significantly reduce recurrence (2
291 an LH surge in response to E + P treatment, LHRH and AVPV neurons in males failed to show increased
293 65% on days 10 and 30, respectively, whereas LHRH-R protein was 64% of control on day 10 and returned
294 nist increases adult height in children with LHRH-dependent precocious puberty and is prescribed by s
298 s that is co-activated to express c-Fos with LHRH neurons at the time of the LH surge, the present st
299 reatment withdrawals were less frequent with LHRH agonists (0% to 4%) than with nonsteroidal antiandr
300 ond to stimulation of AMPARs and mGluRs with LHRH release, and this response is prevented by blocking
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