ライフサイエンスコーパス: hot flush

1 symptoms that occur during a post-menopausal hot flush.

2 sweat rate and cerebral blood flow during a hot flush.

3 e reductions in cerebral blood flow during a hot flush.

4 receptor antagonist (MLE4901) on menopausal hot flushes.

5 e most obvious examples of this condition is hot flushes.

6 ery velocity (MCAv) were measured during the hot flushes.

7 t that NKB signalling may mediate menopausal hot flushes.

8 mood, sleep, sexual function, and nighttime hot flushes.

9 been implicated as an important mediator of hot flushes.

10 sants and antiseizure compounds to alleviate hot flushes.

11 ides new insight into the pathophysiology of hot flushes.

12 demiology, pathophysiology, and treatment of hot flushes.

13 nd other similar compounds can safely reduce hot flushes.

14 he Kupperman Index (KI) and the incidence of hot flushes.

15 adverse events), hypertension (1.2% v 1.0%), hot flushes (0.8% v 0.4%), myalgia (0.8% v 0.7%), dyspne

16 up vs 24 [10%] in the anastrozole group) and hot flushes (26 [11%] in the fulvestrant group vs 24 [10

17 roup), back pain (35 [19%] vs 34 [18%]), and hot flush (27 [15%] vs 21 [11%]); those occurring more f

18 [75%] of 138 in the oestrogen-patch group), hot flushes (44 [56%] vs 35 [25%]), and dermatological p

19 ogen withdrawal in menopausal women leads to hot flushes, a syndrome characterized by the episodic ac

20 Hot flushes affect 70% of menopausal women and often sev

21 Other adverse events included hot flushes, alopecia, abdominal pain, and back pain.

22 toms associated with hypogonadism (nighttime hot flushes and disturbed sleep) increased susceptibilit

23 d bisbenzopyran, was discovered to alleviate hot flushes and effectively increase vaginal fluidity in

24 e longitudinal measurements of the number of hot flushes and night awakenings over time.

25 of breast cancer (in remission) with severe hot flushes and night awakenings were treated with stell

26 Hot flushes and night sweats (HFNS) affect 65-85% of wom

27 ated thermoregulatory dysfunction, including hot flushes and night sweats, is effectively treated by

28 or vasomotor menopausal symptoms (VMSs), ie, hot flushes and night sweats.

29 tion of thermoregulatory mechanisms leads to hot flushes and night sweats.

30 ck can be a safe and effective treatment for hot flushes and sleep dysfunction in this patient popula

31 Debilitating hot flushes and sleep dysfunction often affect survivors

32 survivors of breast cancer with relief from hot flushes and sleep dysfunction with few or no side-ef

33 eas symptoms of estrogen suppression such as hot flushes and sweating were initially more pronounced

34 on tamoxifen plus OFS were more affected by hot flushes and sweats over 5 years than were those on e

35 n agonistic activity on bone, plasma lipids, hot flush, and vagina.

36 ne was associated with a higher incidence of hot flushes, and letrozole was associated with higher in

37 women in the anastrozole group complained of hot flushes at 24 months (23 of 76 [30%] vs 11 of 73 [15

38 affected than patients on tamoxifen alone by hot flushes at 6 and 24 months, by loss of sexual intere

39 en underwent a passive heat stress to induce hot flushes at baseline and follow-up.

40 , disturbed sleep, and more severe nighttime hot flushes, but no significant change in any mood-relat

41 aining reduced the self-reported severity of hot flushes by 109 arbitrary units (80-121, P < 0.001).

42 ificantly reduced the total weekly number of hot flushes by 45 percentage points (95% CI 22-67) compa

43 A post-menopausal hot flush consists of profuse physiological elevations i

44 The total number of hot flushes continued to decrease over the remaining fol

45 The incidence of hot flushes decreased by a maximum of 75% (S21400 lowest

46 The total number of hot flushes decreased from a mean of 79.4 (SD 37.4) per

47 t equal segments, each representing 12.5% of hot flush duration.

48 The primary outcome was the total number of hot flushes during the final week of both treatment peri

49 cal blockade of NKB signalling could inhibit hot flushes during the menopause and during treatment fo

50 most every woman and some men will encounter hot flushes during their lifetime.

51 cacious in a morphine dependent rat model of hot flush efficacy.

52 of menopausal flushing were observed during hot flush episodes.

53 g the trial was not effective in alleviating hot flushes for women in the tamoxifen arm.

54 owever, the effects of NKB administration on hot flushes have not been investigated in humans.

55 constipation, dry mouth, nausea, dizziness, hot flush, headache, hyperhidrosis, and palpitations wer

56 Patients recorded hot flushes in a daily diary by use of the Hot-Flash Sco

57 women aged 40-62 years, having seven or more hot flushes in every 24 h of which some were reported as

58 med to be much more effective in controlling hot flushes in months 6 to 12 in the placebo arm (47.9%

59 human estrogen, 17beta-estradiol, alleviates hot flushes in rat models of thermoregulatory dysfunctio

60 , more women taking HRT at entry experienced hot flushes in the first 6 months than those who did not

61 ail skin temperature (TST) rise representing hot flushes in the morphine-dependent ovariectomized rat

62 e evidence that NKB administration can cause hot flushes in women.

63 The most effective treatments for hot flushes include oestrogens and progestagens.

64 A hot flush is characterised by feelings of intense heat,

65 e physiological responses occurring during a hot flush is currently unknown.

66 ulator (SERM) for the potential treatment of hot flushes is described.

67 e-effects of low testosterone levels such as hot flushes, lack of libido, erectile dysfunction, gynec

68 With the exceptions of hot flushes, libido, and the feeling of being emotionall

69 Training attenuated hot flush MCAv by 3.4 cm s(-1) (0.7-5.1 cm s(-1) , P = 0

70 en who received elagolix had higher rates of hot flushes (mostly mild or moderate), higher levels of

71 24), fatigue (n=23), nipple pain (n=13), and hot flush (n=12), all of which were of mild to moderate

72 Additionally, neither nighttime hot flushes nor disturbed sleep were sufficient to cause

73 arucizumab group (infusion site erythema and hot flushes), one in the 5 g plus 2.5 g idarucizumab gro

74 nd night sweats (problem rating scale of the Hot Flush Rating Scale; P<.001; effect size, 0.39-0.56)

75 ence of the symptoms, the pathophysiology of hot flushes remains unknown.

76 ise training leads to parallel reductions in hot flush severity and within-flush changes in cutaneous

77 Hot flush severity was significantly correlated with dis

78 Exercise training reduces self-reported hot flush severity, but underpinning physiological data

79 esponses can be used to objectively quantify hot flush severity.

80 Women in both groups had similar hot-flush severity and plasma estradiol levels during us

81 igue or asthenia (15 [12%] of 124 patients), hot flush (six [5%]), and decreased appetite (five [4%])

82 Following training, mean hot flush sweat rate decreased by 0.04 mg cm(2) min(-1)

83 anging as it safely and effectively relieves hot flush symptoms without the need for oestrogen exposu

84 lacebo taking HRT at entry experienced fewer hot flushes than women who stopped HRT (22.9% v 34.3%, r

85 strogen-based replacement therapies to treat hot flushes that frequently accompany the transition to

86 neous vasodilatation is a cardinal sign of a hot flush, these results support the hypothesis that KND

87 The number of very severe hot flushes was decreased to near zero by the end of the

88 ekly self-reported frequency and severity of hot flushes were also recorded at baseline and follow-up

89 Severe hot flushes were more strongly related to tamoxifen.

90 Hot flushes were reported more often in the tamoxifen gr

91 elective 17beta-estradiol therapy to relieve hot flushes without undesirable peripheral side-effects.