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 nd other similar compounds can safely reduce hot flushes.

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

6 xifene were nausea, fatigue, arthralgia, and hot flushes.

7 e events were headache, nasopharyngitis, and hot flushes.

8 receptor antagonist (MLE4901) on menopausal hot flushes.

9 been implicated as an important mediator of hot flushes.

10 label placebo (OLP) treatment for menopausal hot flushes.

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

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

13 t that NKB signalling may mediate menopausal hot flushes.

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

15 n effective, safe alternative for menopausal hot flushes.

16 sants and antiseizure compounds to alleviate hot flushes.

17 three [6%]) patients had 50% lesser hot flushes.

18 ides new insight into the pathophysiology of hot flushes.

19 demiology, pathophysiology, and treatment of hot flushes.

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

21 ommonly reported grade 3 adverse events were hot flushes (20 [1%] of 2801 patients in the POAI group

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

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

24 erapy reported moderate to big problems with hot flushes (30.7% [95% CI 29.8-31.6] vs 5.4% [5.0-5.8])

25 st common adverse events up to 24 weeks were hot flushes (35% of participants in PRIMROSE 1 and 32% i

26 [75%] of 138 in the oestrogen-patch group), hot flushes (44 [56%] vs 35 [25%]), and dermatological p

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

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

29 807 patients who received tE2 (p<0.0001) and hot flushes (all grades) in 628 (86%) of those who recei

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

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

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

33 luding fatigue, muscle wastage, weight gain, hot flushes and importantly cognitive impairment, depres

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

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

36 herapist support, on the perceived impact of hot flushes and night sweats (HF/NS) and overall levels

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

38 ymptom Severity Score of moderate and severe hot flushes and night sweats (msVMS-SS) between Q-122 an

39 Menopausal symptoms can extend beyond hot flushes and night sweats (vasomotor symptoms).

40 Vasomotor symptoms (hot flushes and night sweats) are experienced by more th

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

42 VMS, including hot flushes and night sweats, were assessed using the Ko

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

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

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

46 Debilitating hot flushes and sleep dysfunction often affect survivors

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

48 Problem rating of hot flushes and subdomains of quality of life did not im

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

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

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

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

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

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

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

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

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

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

59 o-treatment, OLP reduced the log-transformed hot flush composite score (frequency x intensity) (mean

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

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

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

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

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

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

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

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

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

69 of menopausal flushing were observed during hot flush episodes.

70 s of opioid withdrawal (shortness of breath, hot flushes, fever and pain, small intestinal bleed, and

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

72 0.43; - 0.21], p < 0.001, Cohen's d = 0.86), hot flush frequency (- 1.12 [- 1.81; - 0.43], p = 0.02,

73 for both intervention groups were found for hot flush frequency.

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

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

76 most frequently reported adverse events were hot flush (IM, 7 [10%] vs IA, 14 [21%]) and headache (IM

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

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

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

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

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

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

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

84 Hot flushes (in both trials) and metrorrhagia (in UF-1)

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

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

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

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

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

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

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

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

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

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

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

96 Women with at least five moderate or severe hot flushes per day were allocated to receive four weeks

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

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

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

100 Hot flush severity was significantly correlated with dis

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

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

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

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

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

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

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

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

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

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

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

112 Severe hot flushes were more strongly related to tamoxifen.

113 Hot flushes were reported more often in the tamoxifen gr

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