ライフサイエンスコーパス: sweating

1 ice results in absolute anihidrosis (lack of sweating).

2 s COX-dependent cutaneous vasodilatation and sweating.

3 s unclear whether ET-1 modulates cholinergic sweating.

4 s responses of cutaneous blood flow, but not sweating.

5 timate the amount of water left on skin when sweating.

6 supply is continuous which simulates profuse sweating.

7 ydrated (2.2-5.8% B(m)) via thermoregulatory sweating.

8 ow range in mammals, primarily controlled by sweating.

9 g, and abnormal skin color, temperature, and sweating.

10 ymptoms such as palpitations, dry mouth, and sweating.

11 emperature perception was more impaired than sweating.

12 ise ischaemia contributes to the increase in sweating.

13 y delayed the mean body temperature onset of sweating (+1.24 +/- 0.18 vs. +1.60 +/- 0.18 degrees C, P

14 0.07 degrees C for lidocaine; P = 0.01) and sweating (37.38 +/- 0.09 degrees C for cocaine vs. 37.07

15 adverse events included headache, increased sweating, abdominal pain, and nausea.

16 n, as our ancestors' hair loss increased and sweating ability improved over evolutionary time, the fr

17 model suggests that only when hair loss and sweating ability reach near-modern human levels could ho

18 ce to eye and airway infections and improved sweating ability.

19 tract dysfunction, orthostatic hypotension, sweating abnormalities, or erectile dysfunction.

20 ave provided evidence of viscerally-mediated sweating alterations in humans during exercise brought a

21 primary autonomic defenses against heat are sweating and active precapillary vasodilation; the prima

22 n-flush changes in cutaneous vasodilatation, sweating and cerebral blood flow.

23 During each condition, sweating and cutaneous vascular conductance were measure

24 perosmolality delays the onset threshold for sweating and cutaneous vasodilatation by inhibiting effe

25 , plasma hyperosmolality delays the onset of sweating and cutaneous vasodilatation during heat stress

26 rmal infusion of hyperosmotic saline affects sweating and cutaneous vasodilatation during passive hea

27 n a small dose of intranasal cocaine impairs sweating and cutaneous vasodilation (the major autonomic

28 Effects of blanching, sweating and drying on these characteristics were assess

29 The "wet process", including blanching, sweating and drying, had the largest impact on the compo

30 order characterised by unilateral diminished sweating and flushing of the face in response to heat or

31 g the regulation of cutaneous blood flow and sweating and infer that ET-1 may attenuate the heat loss

32 Acetylcholine elicits sweating and is necessary for development and maintenanc

33 enced more excess salivation, dizziness, and sweating and less dry mouth and decreased appetite than

34 tion revealed fixed dilated pupils, impaired sweating and postural hypotension.

35 Symptoms, heart rate, blood pressure, sweating and skin temperature were compared between NKB

36 ness and attenuate cutaneous vasodilatation, sweating and the reductions in cerebral blood flow durin

37 Eccrine sweat glands are essential for sweating and thermoregulation in humans.

38 vision, severe postural hypotension, reduced sweating and unremitting fever.

39 Temperatures between the sweating and vasoconstriction thresholds define the inte

40 thermoregulatory responses, both autonomic (sweating) and behavioral (peeling off a layer of clothin

41 sturbances, drowsiness or tiredness, nausea, sweating, and being restless or overactive) did not diff

42 h a nasal thermistor); and skin temperature, sweating, and laser-Doppler skin blood flow.

43 mic function measured by pilocarpine-induced sweating, and prevented the loss of nerve fibres in the

44 e elevations in cutaneous vasodilatation and sweating, and reduced brain blood flow.

45 ss responses of cutaneous vasodilatation and sweating, and this may be mediated by prostacyclin-induc

46 Patients with high NO(x) had decreased sweating, and those with suppressed uric acid had decrea

47 tolerated and appeared to alleviate fatigue, sweating, and trouble sleeping.

48 effects of baroreceptor loading/unloading on sweating are less clear.

49 instability, osteopenia, edema, and abnormal sweating-are explicable by small-fiber dysfunction.

50 ajor thermoregulatory defences in humans are sweating, arteriovenous shunt vasoconstriction, and shiv

51 ET-1 does not modulate methacholine-induced sweating at any of the administered concentrations.

52 sion with atropine (0.003 mg ml(-1)) reduced sweating below baseline and blocked pilocarpine-induced

53 ise, the ratio of sweating in the forearm to sweating below the waist was higher in the diabetic pati

54 erienced progressive muscle cramps, profound sweating, bowel disturbances (diarrhoea or constipation)

55 factor, FoxA1, is required to generate mouse sweating capacity.

56 low baseline and blocked pilocarpine-induced sweating completely.

57 Symptoms are protean (flushing, sweating, diarrhea, bronchospasm), usually misdiagnosed,

58 bre loss in conjunction with temperature and sweating dysfunction in familial dysautonomia (FD).

59 blockage, rhinorrhoea, eyelid oedema, facial sweating/flushing and ear flushing.

60 nction, and improvement in neuropathic pain, sweating, gastrointestinal symptoms, hearing loss, and p

61 e regulation of cutaneous vasodilatation and sweating; however, the mechanism(s) underpinning this re

62 of increased heart rate and blood pressure, sweating, hyperthermia, and motor posturing, often in re

63 ir, sparse eyebrows and eyelashes, decreased sweating, hypodontia, and nail anomalies.

64 prosy, and is the first to show that loss of sweating in leprosy may result either from decreased inn

65 These results suggest that sweating in non-glabrous skin during post-IHG exercise i

66 old thresholds at the calf and shoulder, and sweating in response to acetylcholine iontophoresis over

67 diabetic neuropathy typically have decreased sweating in the feet but excessive sweating in the upper

68 The ratio of sweating in the forearm to sweating in the foot was likewise increased in diabetic

69 Likewise, the ratio of sweating in the forearm to sweating below the waist was

70 The ratio of sweating in the forearm to sweating in the foot was like

71 decreased sweating in the feet but excessive sweating in the upper body.

72 that, although prostacyclin does not mediate sweating in young and older males, it does modulate cuta

73 Due to the high rate of secretion, eccrine sweating is a vital regulator of body temperature in res

74 ependent mechanism, and methacholine-induced sweating is not altered by ET-1.

75 that, although prostacyclin does not mediate sweating, it modulates cutaneous vasodilatation to a sim

76 atures included rhinorrhoea, forehead/facial sweating, itching eye, eyelid oedema, sense of aural ful

77 rveillance, UV protection, thermoregulation, sweating, lubrication, pigmentation, the sensations of p

78 a sigmoid dose response curve, with maximal sweating (measured as transepidermal water loss) (mean 7

79 Because excessive sweating of the affected limb is an important feature of

80 wound; chronic pain; extrusion, leakage, or sweating of the implant; necrosis of the nipple, areola,

81 fusion of hyperosmotic saline did not affect sweating or cutaneous vasodilatation.

82 rmal infusion of HYPER saline did not affect sweating (P = 0.99).

83 Like the smart human sweating pores, the flaps can close automatically after

84 ncreased heat storage is mediated by a lower sweating rate (evaporative heat loss) and reduced skin b

85 e and glycopyrrolate increased and decreased sweating, respectively, in 6 month-old controls, db/db m

86 o both whole-body and local heating, whereas sweating responses are preserved.

87 The sweating responses in patients with CHF were not signifi

88 tures include eyelid oedema, forehead/facial sweating, sense of aural fullness and periaural swelling

89 eight loss, abdominal pain, fever, and night sweating should alert physicians to this complication.

90 l elevations in cutaneous vasodilatation and sweating that are accompanied by reduced brain blood flo

91 tes cholinergic cutaneous vasodilatation and sweating through a nitric oxide synthase (NOS)-dependent

92 tes cholinergic cutaneous vasodilatation and sweating through a nitric oxide synthase (NOS)-dependent

93 irectly mediate cutaneous vasodilatation and sweating through nitric oxide synthase (NOS) and calcium

94 idity increases, as might occur during human sweating thus permitting air flow and reducing both the

95 Reduced nicotine-induced axon-reflex sweating was correlated with decreased innervation of sw

96 estrogen suppression such as hot flushes and sweating were initially more pronounced with LAD-3M.