ライフサイエンスコーパス: sweating

1 hould be investigated metabolome-wide after "Sweating".

2 profile variation of S. miltiorrhiza after "Sweating".

3 rhiza showed a significant difference after "Sweating".

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

5 nomic dysfunction, depression, and excessive sweating.

6 al cellulose membrane that responds to human sweating.

7 ndent on sampling materials, approaches, and sweating.

8 s COX-dependent cutaneous vasodilatation and sweating.

9 s unclear whether ET-1 modulates cholinergic sweating.

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

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

12 supply is continuous which simulates profuse sweating.

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

14 ow range in mammals, primarily controlled by sweating.

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

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

17 emperature perception was more impaired than sweating.

18 ise ischaemia contributes to the increase in sweating.

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

20 0.07 degrees C for lidocaine; P = 0.01) and sweating (37.38 +/- 0.09 degrees C for cocaine vs. 37.07

21 "Sweating", a processing method of Traditional Chinese Me

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

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

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

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

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

27 Fabrication of the sweating actuator usually takes 3-6 h, depending on size

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

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

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

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

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

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

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

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

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

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

38 nd left flank abdominal pain, accompanied by sweating and fatigue.

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

40 Sweating and heat buildup at the skin-liner interface is

41 -T(4) sympathicotomy, with less compensatory sweating and higher patients' satisfaction.

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

43 Acetylcholine elicits sweating and is necessary for development and maintenanc

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

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

46 heating layer that serves to both stimulate sweating and prevent saturation of the sensing area, red

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

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

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

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

51 Temperatures between the sweating and vasoconstriction thresholds define the inte

52 a causes mild symptoms like fever, headache, sweating and vomiting, and muscle discomfort; severe sym

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

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

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

56 ivities, stress events, hypoglycemia-induced sweating, and Parkinson's disease.

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

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

59 ifests as elevated skin temperature, lack of sweating, and seizures.

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

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

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

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

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

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

66 cantly attenuated (p = 0.0002) and perceived sweating, as reported by prosthesis users, improved (p =

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

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

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

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

71 s than in other apes despite humans' greater sweating capacity.

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

73 low baseline and blocked pilocarpine-induced sweating completely.

74 om 13 millimeters (under low humidity and no sweating conditions) to 2 millimeters (under high humidi

75 s) to 2 millimeters (under high humidity and sweating conditions), expanding the thermal regulation c

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

77 It should be noted that sweating does not weaken the piezoelectric properties of

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

79 s, increased exercise duration and increased sweating fluid and ion losses during submaximal exercise

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

81 Hyperhidrosis, excessive sweating from the eccrine sweat glands, is caused by ove

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

83 We conclude that "Sweating'' has significant effect on metabolites content

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

85 pical applied Tris-BNPs were not affected by sweating, humidity, or active wiping due to their prefer

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

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

88 s suffer from itching, recurrent infections, sweating impairment (hypohidrosis) with heat intolerance

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

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

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

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

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

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

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

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

97 - secretion in sweat gland cells and reduces sweating in vivo in mice, showing that Ca2+ tunneling is

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

99 curs in older individuals, is exacerbated by sweating, irradiation, cancers, medications, kidney fail

100 Sweating is a basic skin function in body temperature co

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

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

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

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

105 reased exercise duration, despite continuing sweating losses of fluid and ions.

106 ellular fluid shifts, as well as significant sweating losses of water and ions.

107 oral supplementation can effectively offset sweating losses.

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

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

110 interrogated gene function for roles in the sweating mechanism.

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

112 lary, and/or palmar hyperhidrosis (excessive sweating of the face, armpits, and hands) has a reported

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

114 e of heat-non-conducting materials may cause sweating of the residual limb and may result in liners s

115 After ramicotomy, some residual sweating on the face, hands, and axillae.

116 hoeic athletes, chronic OCP use impaired the sweating onset threshold and thermosensitivity (both P <

117 orrhoea OR 2.65, 95% CI 1.26 to 5.86; facial sweating OR 2.53, 95% CI 1.33 to 4.93).

118 while holding an object, for example, due to sweating or condensation.

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

120 ion and fur growth, short-term shivering and sweating or panting, and movement between warm and cold

121 wing to an orthogonal mechanism; the gradual sweating-out of residual low molecular weight solvent mo

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

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

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

125 tenuated body fluid losses while maintaining sweating rates.

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

127 and also that chronic OCP use attenuates the sweating response, whereas behavioural thermoregulation

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

129 The sweating responses in patients with CHF were not signifi

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

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

132 at consumption than cotton in the artificial sweating skin test.

133 ads into niche applications involving active sweating, such as hydration monitoring for athletes and

134 Patient symptoms (mood, sweating, temperature, and oculogyric crises), patient g

135 Focus on the sweating, temperature, quality of life baseline and post

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

137 fibres and we effectively dissipate through sweating the metabolic heat generated through prolonged,

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

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

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

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

142 cluding tachycardia, hypertension, flushing, sweating, warmth, coldness, nausea, phosphenes, and fear

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

144 The response to exercise-induced sweating was significantly different to chemically-induc

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

146 ignificantly different to chemically-induced sweating where the sweat chloride concentration was almo

147 Compensatory sweating worse with sympathicotomy.