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1 nd the glucocorticoid receptor (GR) in fetal hypothalami.
2 reased expression of STAT3 protein in mutant hypothalami, but does not lead to obesity.
3 ctor (FSHRF) was purified from rat and sheep hypothalami, but has not been isolated.
4 of neurons, we generated physically chimeric hypothalami by microtransplanting small numbers of embry
5 plant cultures from postnatal, preoptic area/hypothalami, containing three anatomically discrete DA p
6                               The mediobasal hypothalami from adult male rats were incubated in an in
7                                              Hypothalami from five adult males were frozen in isopent
8  of hypocretin-producing cells in postmortem hypothalami from narcoleptic individuals was reported.
9 GLUT1, GLUT2 and GLUT4 in frozen sections of hypothalami from normal rats.
10                                          The hypothalami from ovariectomized rats, treated with eithe
11    Comparative in situ analysis of slices of hypothalami generated from control and leptin-injected o
12 ach to quantify endogenous peptide levels in hypothalami of animals subjected to different diets reve
13 e diet for 4 days, the content of ATP in the hypothalami of control i.c.v. injected animals fell by 3
14 , Nhlh2 and Pcsk1 expression were reduced in hypothalami of fasted Snord116 paternal knockout (Snord1
15 nscript (CART)] neuropeptide messages in the hypothalami of lean and obese (ob/ob) mice.
16 easing hormone (GnRH) was carried out on the hypothalami of male and female rats.
17 ermine levels of messenger RNA (mRNA) in the hypothalami of mice at different ages.
18              Gene set enrichment analysis in hypothalami of mice with sodium appetite showed signific
19 oth in GT1-7 hypothalamic neurons and in the hypothalami of mice.
20 ulation of anorexigenic neuropeptides in the hypothalami of mice.
21 pattern of core clock gene expression in the hypothalami of mice.
22 al cilia lengths were selectively reduced in hypothalami of obese mice with leptin deficiency and lep
23 g, leptin-responsive hypothalamic cells into hypothalami of postnatal leptin receptor-deficient (db/d
24 al stem cells and transplanted them into the hypothalami of rats subjected to breast carcinogenesis.
25  were markedly reduced at these times in the hypothalami of VMH-lesioned rats.
26 egions, including the anterior and posterior hypothalami (regions long associated with body temperatu
27 2.) After determining the basal release, the hypothalami were challenged with 0, 0.1, 1 or 10 nm of l
28                                              Hypothalami were sectioned, immunocytochemically stained
29 ty-one days after SC, rats were perfused and hypothalami were serially sectioned and alternately stai
30                      Moreover, incubation of hypothalami with 10 nM of leptin and bicuculline, a comp
31  GAD levels was examined by incubating basal hypothalami with D-oligos in vitro and subsequent Wester

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