ライフサイエンスコーパス: GH deficiency

1 acute lymphoblastic leukemia (ALL) who have GH deficiency.

2 endocrinology, including in patients without GH deficiency.

3 rves with a genetic mutation that results in GH deficiency.

4 e short stature secondary to growth hormone (GH) deficiency.

5 ad hyperprolactinemia, 2 had growth hormone (GH) deficiency, 1 had adrenocorticotropic hormone (ACTH)

6 is decreased in WAT from mice with isolated GH deficiency, 2) is increased in WAT from mice with chr

7 is complex, and is dependent on the onset of GH deficiency, age of the patient and dosing regimen.

8 The possibility of adult GH deficiency (AGHD) should always be considered in indi

9 t of POU1F1 in dominantly inherited isolated GH deficiency and demonstrates a significant impact of t

10 Growth hormone (GH) deficiency and loss of physical activity are common

11 formation of pituitary Rathke's cleft cysts, GH deficiency, and short stature provide a model to stud

12 Growth impairment and growth hormone (GH) deficiency are complications after total body irradi

13 PI 3-kinase activity was robust in mice with GH deficiency, but not in mice with GH excess.

14 ne and (ii) mutations of these repeats cause GH deficiency by perturbing alternative splicing.

15 tients compared with healthy subjects; thus, GH deficiency does not account for rheumatoid cachexia.

16 al models and human diseases shows that both GH deficiency (GHD) and excess are associated with chang

17 d for use to promote growth in children with GH deficiency (GHD), along with several additional clini

18 Growth hormone (GH) deficiency (GHD) in children is defined as impaired

19 ture in the following areas: growth hormone (GH) deficiency, gonadotropin-releasing hormone (GnRH) an

20 Some patients with growth hormone (GH) deficiency have mutations in the GH-releasing hormon

21 An autosomal dominant form of isolated GH deficiency (IGHD-II) is caused by mutations in IVS3 o

22 GH deficiency in adulthood causes a distinct syndrome wi

23 mutations segregated with autosomal dominant GH deficiency in both kindreds and no other allelic GH g

24 produced preferentially in the situation of GH deficiency in contrast to the pattern in the GH-suffi

25 e increased GRF expression which accompanies GH deficiency in other dwarf rats.

26 s safe and efficacious for the correction of GH deficiency in survivors of childhood ALL.

27 Growth hormone (GH) deficiency is associated with increased cardiovascul

28 Primary growth hormone (GH) deficiency is associated with MASLD, and the decline

29 ated abdominal fat accumulation and relative GH deficiency, low-dose GH received for 18 months result

30 amined the in vivo effect of growth hormone (GH) deficiency on the expression of KBP in the Lewis dwa

31 d in individuals with a history of childhood GH deficiency or significant hypothalamic-pituitary dama

32 lications, whereas individuals with isolated GH deficiency such as Laron dwarfs show increased life s

33 ngitis virus (LCMV) causes a growth hormone (GH) deficiency syndrome (GHDS) manifested as growth reta

34 erminants contribute to this growth hormone (GH) deficiency syndrome (GHDS).

35 tandard deviation (SD) from the diagnosis of GH deficiency to the achievement of final height were co

36 tions for GH therapy in 78% of children with GH deficiency, Turner syndrome, or renal failure; of tho

37 After HCT, GH deficiency was diagnosed at 1.5 years (range, 0.8-9.5

38 After pituitary GH deficiency was excluded, subjects underwent arginine

39 atients undergoing GH therapy have classical GH deficiency, while 42% have other conditions.