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1 acute lymphoblastic leukemia (ALL) who have GH deficiency.
2 rves with a genetic mutation that results in GH deficiency.
3 e short stature secondary to growth hormone (GH) deficiency.
4 ad hyperprolactinemia, 2 had growth hormone (GH) deficiency, 1 had adrenocorticotropic hormone (ACTH)
5 is decreased in WAT from mice with isolated GH deficiency, 2) is increased in WAT from mice with chr
6 is complex, and is dependent on the onset of GH deficiency, age of the patient and dosing regimen.
8 t of POU1F1 in dominantly inherited isolated GH deficiency and demonstrates a significant impact of t
9 formation of pituitary Rathke's cleft cysts, GH deficiency, and short stature provide a model to stud
13 tients compared with healthy subjects; thus, GH deficiency does not account for rheumatoid cachexia.
14 ture in the following areas: growth hormone (GH) deficiency, gonadotropin-releasing hormone (GnRH) an
18 mutations segregated with autosomal dominant GH deficiency in both kindreds and no other allelic GH g
19 produced preferentially in the situation of GH deficiency in contrast to the pattern in the GH-suffi
23 ated abdominal fat accumulation and relative GH deficiency, low-dose GH received for 18 months result
24 amined the in vivo effect of growth hormone (GH) deficiency on the expression of KBP in the Lewis dwa
25 d in individuals with a history of childhood GH deficiency or significant hypothalamic-pituitary dama
26 lications, whereas individuals with isolated GH deficiency such as Laron dwarfs show increased life s
27 ngitis virus (LCMV) causes a growth hormone (GH) deficiency syndrome (GHDS) manifested as growth reta
29 tandard deviation (SD) from the diagnosis of GH deficiency to the achievement of final height were co
30 tions for GH therapy in 78% of children with GH deficiency, Turner syndrome, or renal failure; of tho
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