ライフサイエンスコーパス: hyperandrogenism

1 e mild non-classic form is a common cause of hyperandrogenism.

2 the pathogenesis of "polycystic" ovaries in hyperandrogenism.

3 hrome P450c17 alpha activity and ameliorates hyperandrogenism.

4 ical hyperandrogenism as opposed to clinical hyperandrogenism alone showed a metabolic phenotype (p <

5 valent but unreliable markers of biochemical hyperandrogenism among this population.

6 ndocrine disorder of women, characterized by hyperandrogenism and chronic anovulation.

7 dition in which intrinsic functional ovarian hyperandrogenism and excess adiposity share a common ori

8 he proposed "vicious cycle" model integrates hyperandrogenism and hyperinsulinemia in peripheral insu

9 insight into the fetal loss associated with hyperandrogenism and insulin resistance in women and sug

10 ults suggest that the deleterious effects of hyperandrogenism and insulin resistance on fetal surviva

11 HT) and insulin to investigate the impact of hyperandrogenism and insulin resistance on fetal surviva

12 ulin exhibited endocrine aberrations such as hyperandrogenism and insulin resistance that are strikin

13 ydrotestosterone (DHT) and insulin exhibited hyperandrogenism and insulin resistance, as well as incr

14 late childhood or early adulthood with mild hyperandrogenism and is an important cause of masculiniz

15 case group included girls with high (n = 40, hyperandrogenism and oligomenorrhea or amenorrhea), inte

16 pathway linking hyperinsulinism with ovarian hyperandrogenism and the infertility of obesity.

17 ncluding acanthosis nigricans, organomegaly, hyperandrogenism, and diabetes.

18 Insulin resistance and hyperandrogenism are the cardinal features of polycystic

19 COS women with both biochemical and clinical hyperandrogenism as opposed to clinical hyperandrogenism

20 sorder of unknown aetiology characterized by hyperandrogenism, chronic anovulation and defects in glu

21 In summary, excess NR5A1 expression causes hyperandrogenism, disruption of ovarian functions, prema

22 sfunction (cycle length < 21 or >= 35 days), hyperandrogenism (free testosterone concentration > 75th

23 is often complicated by inadequately treated hyperandrogenism, iatrogenic hypercortisolism, or both.

24 ch and whether preclinical work is modelling hyperandrogenism in physiologically relevant terms for P

25 an experience iatrogenic Cushing's syndrome, hyperandrogenism, infertility, or the development of the

26 Hyperandrogenism is a key feature together with lower le

27 Gestational hyperandrogenism is a risk factor for adverse maternal a

28 Gestational hyperandrogenism is once such adverse in-utero insult.

29 Clinical and/or biochemical hyperandrogenism is one of the diagnostic criteria for P

30 Hyperandrogenism is the most consistent PCOS characteris

31 As such, hyperandrogenism is the proposed locus of origin for the

32 racterized by irregular menstrual cycles and hyperandrogenism, is a common ovulatory disorder.

33 (T)-treatment, an environment of gestational hyperandrogenism, manifests as hypertension and patholog

34 ent etiologies of type 2 diabetes, such that hyperandrogenism may increase risk in women while decrea

35 -PCOS subgroup) had oligomenorrhea (n = 75), hyperandrogenism (n = 257), or polycystic ovarian morpho

36 ray of disorders, including oligo-ovulation, hyperandrogenism, obesity, hyperlipidemia, infertility a

37 The ordinary hypergonadotropic hyperandrogenism of obese women appears to be an excepti

38 matched (+/- 2 years) girls with no clinical hyperandrogenism, oligomenorrhea, or amenorrhea.

39 a-based PCOS, women with partial phenotypes (hyperandrogenism, oligomenorrhea, or polycystic morpholo

40 oint was development of PCOS components (ie, hyperandrogenism or ovulatory dysfunction).

41 Rotterdam criteria (anovulation with either hyperandrogenism or polycystic ovaries).

42 norrhea or amenorrhea), intermediate (n = 8, hyperandrogenism), or low (n = 7, oligomenorrhea or amen

43 rimary hyperaldosteronism, hypercortisolism, hyperandrogenism, or hyperestrogenism), and less than 1%

44 of three criteria - clinical or biochemical hyperandrogenism, ovulatory dysfunction, and/or specific

45 lin receptor (INSR) mutations develop severe hyperandrogenism secondary to hyperinsulinaemia.

46 y be associated with adverse birth outcomes, hyperandrogenism, sexual dysfunction, and impaired impla

47 PCOS, marked by insulin resistance and hyperandrogenism, strongly contributes to early-onset ty

48 rome (PCOS) that, alongside subfertility and hyperandrogenism, typically presents with increased lute

49 tionally relevant ovine model of gestational hyperandrogenism we have previously reported cardiometab

50 stic ovary syndrome's (PCOS) main feature is hyperandrogenism, which is linked to a higher risk of me

51 We hypothesized that gestational hyperandrogenism would lead to sex-specific disruption i