ライフサイエンスコーパス: subfertility

1 , contribute to epididymal damage, and drive subfertility.

2 e-/- animals as a key contributing factor to subfertility.

3 lower testis weight, lower sperm count, and subfertility.

4 efficiency in mice, resulting in severe male subfertility.

5 ly depletion of ovarian follicles and female subfertility.

6 le mice heterozygous for Gpx4_U46S presented subfertility.

7 nic anomalies, diminished sperm motility and subfertility.

8 hypoplasia, eyelid abnormalities and female subfertility.

9 number of cycles before reaching a metric of subfertility.

10 of RAMP2 (but not RAMP3) display remarkable subfertility.

11 disease, appendectomy, and interventions for subfertility.

12 thylation, and are not explained by parental subfertility.

13 .13]) were associated with increased odds of subfertility.

14 een PUFA(-rich foods) with fecundability and subfertility.

15 Fertility trials also indicated severe subfertility.

16 ted with increased fecundability and reduced subfertility.

17 ntrol for family confounding factors such as subfertility.

18 by resulting in asthenozoospermia and severe subfertility.

19 estis weight, decreased sperm count and male subfertility.

20 atory tract disease, laterality defects, and subfertility.

21 ultimately resulting in sperm DNA damage and subfertility.

22 ty data identified a dairy bull with extreme subfertility (10% pregnancy rate).

23 ed conception, 141 180 (10.3%) with parental subfertility, 20 429 (1.5%) following OI or IUI, and 23

24 infertility without fertility treatment (ie, subfertility), (3) ovulation induction (OI) or intrauter

25 rther increases in birth rates in women with subfertility, a greater awareness of lifestyle factors a

26 Finally, associations between male subfertility and a spectrum of health-threatening condit

27 ee analysis to estimate threshold values for subfertility and fertility with respect to the sperm con

28 cystic ovary syndrome (PCOS) that, alongside subfertility and hyperandrogenism, typically presents wi

29 ated loss of the ovarian reserve, leading to subfertility and infertility.

30 in the range of reproductive failure linking subfertility and late pregnancy complications and has al

31 eproductive defects in mice including female subfertility and male infertility.

32 has important implications for the roles of subfertility and manipulation by nest mates in the evolu

33 However, single ablation of Igf1r leads to subfertility and mice lacking both receptors are inferti

34 and social disadvantage are associated with subfertility and miscarriage risks.

35 tion, defined as (1) natural conception, (2) subfertility and non-ART (ie, infertility diagnosis but

36 Subfertility and severe pelvic pains are symptoms associ

37 l core outcomes (for example, heart failure, subfertility and subsequent neoplasms) and three aspects

38 yndrome, ophthalmoplegia, parkinsonism, male subfertility and, in a transgenic mouse model, premature

39 vy menstrual bleeding, abdominal discomfort, subfertility, and a reduced quality of life.

40 ion in women that results in pelvic pain and subfertility, and has been associated with decreased bod

41 idualization-based recurrent pregnancy loss, subfertility, and infertility.

42 Infertility and subfertility are important and pervasive reproductive pr

43 Indeed, current generations of couples with subfertility are more fortunate than previous generation

44 he probability of conceiving within 1 mo and subfertility as time to pregnancy >=12 mo or use of assi

45 YAP1 is a promising target for treatment of subfertility associated with abnormal granulosa cell fun

46 ofWnt5a(but notWnt11) results in the female subfertility associated with increased follicular atresi

47 gral to treating prostate and breast cancer, subfertility, blood pressure, and other diseases.

48 h lower fecundability and increased risks of subfertility but not with miscarriage risk.

49 s impairs spermatogenesis, resulting in male subfertility, but causes no meiotic arrest.

50 nsgenic animals demonstrate reduced fitness, subfertility, defective meiotic pairing, and other germ-

51 as the per-month probability of conceiving; subfertility, defined as a time to pregnancy or the dura

52 he probability of conceiving within 1 month; subfertility, defined as time to pregnancy or duration o

53 ubunit (PPP4C) deletion causes severe female subfertility due to accumulation of DNA damage in oocyte

54 ce using CRISPR/Cas9 which results in female subfertility due to delayed GVBD.

55 on-neuronal brain cells are known to exhibit subfertility due to hypogonadotropic hypogonadism.

56 These results suggest that subfertility exhibited by female mice following Chst10 l

57 iated with increased fecundability and lower subfertility (FR: 1.10, 95% CI: 1.01, 1.20; OR: 0.78, 95

58 rt that HELQ helicase-deficient mice exhibit subfertility, germ cell attrition, ICL sensitivity and t

59 for ASD was 1.20 (95% CI, 1.15-1.25) in the subfertility group, 1.21 (95% CI, 1.09-1.34) following O

60 ed conception group, 33.3 (4.7) years in the subfertility group, 33.1 (4.4) years in the OI or IUI gr

61 I), a common cause of female infertility and subfertility, has a well-established hereditary componen

62 er associated with menstrual irregularities, subfertility, hirsutism, acne, and a range of endocrine

63 eutral lipid- and LD-associated genes causes subfertility; however, key regulators of testis neutral

64 increased risks of spontaneous abortion and subfertility (i.e., taking more than 1 year of unprotect

65 a-3 and omega-6 PUFAs with fecundability and subfertility in females and males.

66 gest FOXA3 as a potential candidate gene for subfertility in man.

67 hic sperm motility defects resulting in male subfertility in the human population.

68 of corpora lutea, reduced ovarian size, and subfertility in transgenic mice.

69 ven the need to find efficient treatments of subfertility in women, our results should be confirmed i

70 for some of the unexplained infertility (or subfertility) in the general population.

71 common endocrine disorder, characterized by subfertility, increased risk of metabolic diseases, and

72 ivation of the Alox15 gene might rescue male subfertility induced by heterozygous expression of catal

73 We further demonstrate that male subfertility is associated with a decrease in metals zin

74 diagnostic evaluation and treatment of male subfertility is beneficial for most physicians.

75 icient mouse model, we demonstrate that male subfertility is caused by sterile epididymitis character

76 Subfertility is common and affects one in six couples, h

77 Female subfertility is highly associated with endometriosis.

78 The timely access to effective treatment for subfertility is important as many couples have a narrow

79 Male subfertility is often correctable, may be genetically tr

80 in, it is currently unclear whether diabetic subfertility is the result of deficiency of pancreatic i

81 epubertal boys suffering from infertility or subfertility later in life.

82 pportunity before the age-related effects of subfertility limit the likelihood of success.

83 Underlying parental characteristics and subfertility may also play a role.

84 from which a couple is drawn and the precise subfertility metric which is most relevant, for example

85 productive technologies for the treatment of subfertility, more men are fathering children at advance

86 there was a nonsignificant increased risk of subfertility (odds ratio in the high exposure group = 1.

87 8; 95% confidence interval (CI) 1.4-5.6) and subfertility (odds ratio in the high exposure group = 4.

88 ially how selection would favor sterility or subfertility of most individuals within a highly social

89 Individuals with subfertility or fertility treatment were older and resid

90 eifers, classified as having high fertility, subfertility or infertility, were selected for further s

91 osis are chronic intolerable pelvic pain and subfertility or infertility, which profoundly affect the

92 emature depletion of the PF reserve leads to subfertility or infertility.

93 besity was associated with increased odds of subfertility (OR, 1.69 [95% CI, 1.24-2.31]).

94 n age at first birth, increased treatment of subfertility, or changes in oral contraceptive use.

95 velopments in the diagnosis and treatment of subfertility over the past 50 years have been truly rema

96 or (Pgr)-expressing cells resulted in female subfertility, partially due to an embryo developmental d

97 ious retinal pathology but leads to a severe subfertility phenotype in agreement with minor endogenou

98 To characterize the subfertility phenotype, a range of in vitro, in vivo, an

99 d Ca(2+) responses, reduced AE, and a strong subfertility phenotype.

100 Ovarian infertility and subfertility presenting with premature ovarian insuffici

101 in sperm flagella can cause female and male subfertility, respectively, and malfunctional motile mon

102 ample, poverty was associated with increased subfertility risk (32.5% vs 50.3%; relative risk, 1.37 [

103 iated with increased fecundability and lower subfertility risk [fecundability ratio (FR): 0.92, 95% c

104 Our results demonstrate that the subfertility seen in male PLAG1-deficient mice is, at le

105 esulting in more pronounced deficiencies and subfertility, suggesting the Arp2 paralogs are cross-spe

106 n-54 can induce egg maturation in women with subfertility undergoing in vitro fertilization therapy.

107 Causes of male subfertility vary highly, but can be related to congenit

108 cycles of non-conception as an indicator of subfertility was found to be reasonably robust, though a

109 Subfertility was manifested in a reduced number of litte

110 rtility was seen in 79 patients (17.6%), and subfertility was seen in nine patients (2%).

111 The effect estimates of subfertility were in line with those for fecundability;

112 Cylc1 deficiency resulted in male subfertility, whereas Cylc2(-/-), Cylc1(-/y)Cylc2(+/-),

113 (hazard ratio, 1.58; 95% CI, 1.17-2.12) and subfertility with non-ART conception (hazard ratio, 1.42