ライフサイエンスコーパス: cold exposure

1 ic metabolism in adipose depots during acute cold exposure.

2 me severely hypothermic and succumb to acute cold exposure.

3 ere mostly less abundant after both salt and cold exposure.

4 roteins after salt exposure when compared to cold exposure.

5 diture increased to similar levels as during cold exposure.

6 l for appropriate thermogenic response after cold exposure.

7 s stimulated by fever-inducing endotoxins or cold exposure.

8 ng H3K27me3 marks depending on the length of cold exposure.

9 rature and thus are unable to adapt to acute cold exposure.

10 r pharmacological beta-adrenergic agonism or cold exposure.

11 450 h CR) trees under controlled-environment cold exposure.

12 he level of chromatin triggered by long-term cold exposure.

13 luding reduced ATP levels and intolerance to cold exposure.

14 greater skin blood flow and heat loss during cold exposure.

15 y were adults, measured T(IBAT) during acute cold exposure.

16 e is reduced and remains unchanged following cold exposure.

17 pisodes of rash, arthralgia, and fever after cold exposure.

18 that the control was non-adaptive on chronic cold exposure.

19 ng sympathetic premotor neurons activated by cold exposure.

20 ergo specific metabolic changes during acute cold exposure.

21 es of caloric deficiency, leptin, obesity or cold exposure.

22 ratios and provides metabolic savings during cold exposure.

23 athione peroxidase expression increased with cold exposure.

24 ses to fasting, stress, thyroid hormone, and cold exposure.

25 n increased by 1.8-fold in response to acute cold exposure.

26 e was normal, and they responded normally to cold exposure.

27 rns to normal shortly after cessation of the cold exposure.

28 , which appears to depend on the duration of cold exposure.

29 por nearly continuously throughout 2.5 yr of cold exposure.

30 ed during the initial rewarming period after cold exposure.

31 NA is increased 30-fold in BAT within 6 h of cold exposure.

32 nalysis to identify cDNAs rapidly induced by cold exposure.

33 eserve glucose homeostasis in the setting of cold exposure.

34 s were monitored during moderate and extreme cold exposure.

35 , both among treatments and before and after cold exposure.

36 nd Ucp1 expression in the WAT in response to cold exposure.

37 rature compared to UCP1KO alone during acute cold exposure.

38 hard reset in a defibrillator as a result of cold exposure.

39 strate the distinct metabolism of BAT during cold exposure.

40 SPECT/CT after an overnight fast and 2 h of cold exposure.

41 vere defect in BAT oxidative metabolism upon cold exposure.

42 35-37 degrees C) during the entire period of cold exposure.

43 ients with type 2 diabetes during controlled cold exposure.

44 t not distal tibial, MAT is lost with 21-day cold exposure.

45 creates a partially vernalized state without cold exposure.

46 le after exercise and in adipose tissue upon cold exposure.

47 alpine habitats must retreat to avoid lethal cold exposure.

48 teristic of brown fat and were intolerant to cold exposure.

49 rates transcriptional shutdown of FLC during cold exposure.

50 otect their core temperatures in response to cold exposure.

51 development, high-fat diet (HFD) feeding and cold exposure.

52 isualized using (18)F-FDG PET/CT during mild cold exposure.

53 ases disproportionately during environmental cold exposure.

54 s they aged and developed hypothermia during cold exposure.

55 yed substantial NEFA and glucose uptake upon cold exposure.

56 itter release to brown adipose tissue during cold exposure.

57 e single and DKO mice to acute and long-term cold exposures.

58 ambient conditions (22 degrees C) and acute cold exposure (12 degrees C for 24 hours).

59 zone (TNZ, 30 degrees C) for mice or during cold exposure (15 degrees C) in male wild-type mice.

60 After 1 h of cold exposure, (18)F-FDG (one occasion) or (123)I-MIBG (

61 in situ hybridization, we found that chronic cold exposure (20 days at 4oC) increased arcuate nucleus

62 During extreme cold exposure (21 degrees C < or = air temperature < or

63 C is mediated by alpha2A-ARs, whereas after cold exposure (28 degrees C), alpha2C-ARs are no longer

64 During moderate cold exposure (30 degrees C < or = air temperature < or

65 Previous studies have demonstrated that cold exposure (4 degrees C) blocks permeability barrier

66 BAT under control conditions (22 degrees C), cold exposure (4 degrees C, 1 to 48 h), warm acclimation

67 xpression with fasting, leptin treatment and cold exposure (4 h at 4 degrees C) and found no change,

68 d hypertension (CIH) induced by six weeks of cold exposure (6 degrees C).

69 Chronic cold exposure (7 days, 4 h/day, 4 degrees C) potentiated

70 both Trpa1(-/-) and Trpa1(+/+) mice, severe cold exposure (8 degrees C) resulted in decreases of ski

71 During cold exposure, a gene encoding a unique, cold-specific P

72 certain environmental cues, such as chronic cold exposure, a process often referred to as "browning"

73 val for early deliveries associated with hot/cold exposures, adjusting for conception month, humidity

74 been recently shown that in response to mild cold exposure, adult human BAT consumes more glucose per

75 tion of the migration cycle, because without cold exposure, aged migrants continue to orient south.

76 Cold exposure also increased blood pressure and energy e

77 thermogenesis, their sleep behaviors during cold exposure also were examined.

78 ategory level also differed between salt and cold exposure although common trends, previously describ

79 including thermogenic responses to diet and cold exposure and 'beiging' of white adipose tissue.

80 Moreover, cold exposure and beta3-adrenergic receptor signaling, c

81 rol of adaptive thermogenesis in response to cold exposure and diet, 2) control of reactive oxygen sp

82 y regulated in the brown adipose tissue upon cold exposure and during brown fat cell differentiation.

83 eposition on FLC chromatin in the absence of cold exposure and enhanced H3K27me3 spreading during col

84 o determine whether this discrepancy between cold exposure and foot shock might be related to differe

85 nction in the measurement of the duration of cold exposure and in the establishment of the vernalized

86 understanding of the importance of TRPA1 in cold exposure and provide impetus for further research i

87 tivators of brown adipose tissue (BAT), mild cold exposure and sympathomimetic drugs have been consid

88 except that symptoms are not precipitated by cold exposure and that sensorineural hearing loss is fre

89 d the cardiovascular consequences of extreme cold exposure and their relationship with ultrasound pro

90 ow loss of UCP1 or SLN is compensated during cold exposure and whether they are both necessary for th

91 control conditions, during acute and chronic cold exposure, and during chronic adrenergic stimulation

92 itochondrial ROS results in hypothermia upon cold exposure, and inhibits UCP1-dependent increases in

93 on appears to be activated on demand, during cold exposure, and parallels the tonic inhibitory GABAer

94 mutant, resulting in rapid flowering without cold exposure, and the rapid-flowering rvr1 phenotype is

95 Collectively, these results identify cold exposure as a natural stimulus for OEA formation in

96 the brain in this coupling process, we used cold exposure as an experimental paradigm because the sy

97 [BdVRN2L]), and FT before, during, and after cold exposure as well as in different photoperiods.

98 d to maintain a normal body temperature upon cold exposure because of limited fuel supplies.

99 antagonist had impaired heat production upon cold exposure, but no change in basal temperature and no

100 Cold exposure can enhance energy expenditure by activati

101 utral conditions and after prolonged (5-8 h) cold exposure (CE).

102 mory of cold is digital: following long-term cold exposure, cells respond autonomously in an all-or-n

103 loss of body temperature and survival after cold exposure compared to UCP1KO mice.

104 ) turnover in 6 healthy men under controlled cold exposure conditions.

105 (2.42 +/- 0.85 vs. 3.43 +/- 0.93, P = 0.02), cold exposure decreased the (11)C-HED RI in WAT (0.44 +/

106 ese experiments suggest that, during extreme cold exposure, decreased cardiac output and increased bl

107 Glp1r(-/-) mice exhibit a normal response to cold exposure, demonstrating that endogenous GLP-1R sign

108 -matched control subjects under experimental cold exposure designed to minimize shivering.

109 nist at 30 mg/kg before severe (3 degrees C) cold exposure did not affect the thermoregulatory respon

110 ase energy expenditure to the same extent as cold exposure does not activate BAT in humans, indicatin

111 time span of which increases with increasing cold exposure duration and closely matches the duration

112 flowering locus C (FLC) increasing with the cold exposure duration.

113 Additionally, cold exposure elevates SIRT2 expression in brown adipose

114 a produced similar activations of BAT during cold exposure, following a brain transection caudal to t

115 phyxia (100% N(2) for 50 seconds followed by cold exposure for 10 minutes).

116 sed in brown adipocytes by norepinephrine or cold exposure, further amplifying the increase in D2 act

117 of age and do not huddle effectively during cold exposure, gaining little thermoregulatory benefit f

118 These data suggest that in the absence of cold exposure, GPAT4 limits excessive fatty acid oxidati

119 indicates that habituation to repeated short cold exposures has a cross-adaptive effect during hypoxi

120 s of the inputs that activate the RMR during cold exposure have not been definitively identified.

121 atically distinct metabolic responses during cold exposure in BAT and WAT.

122 n this study, we sought to determine whether cold exposure in early neonatal life could induce enhanc

123 mmatory mechanisms occurring after a general cold exposure in FCAS patients and to investigate the ef

124 ain high rates of myoclonic twitching during cold exposure in infant rats.

125 ls correlated with BAT activity during acute cold exposure in male subjects.

126 Thermogenesis against cold exposure in mammals occurs in brown adipose tissue

127 Acute cold exposure in mature animals augments BAT thermogenes

128 Here we report that cold exposure in mice triggers a metabolic program that

129 gulated in brown and white adipose following cold exposure in mice, highlighting a potential role in

130 aracterize the initial metabolic response to cold exposure in multiple adipose tissue depots in mice.

131 daptive metabolic response to starvation and cold exposure in peripheral tissues.

132 Cold exposure in potato resulted in a higher number of s

133 nability to maintain body temperature during cold exposure in Ppt1-KO mice was associated with an ade

134 concomitants of ultrasound production during cold exposure in rats pretreated with saline or the gang

135 AT) is vital for proper thermogenesis during cold exposure in rodents, but until recently its presenc

136 mmed in the seed to ensure a requirement for cold exposure in the next generation.

137 anisms underlying homeostatic failure during cold exposure in this diverse group of ectotherms.

138 In the present studies, cold exposure increased Dio2(-/-) BAT sympathetic stimul

139 n interscapular brown adipose tissue (iBAT), cold exposure increased proliferation of endothelial cel

140 Here we show that cold exposure increases OEA levels in rat white adipose

141 to the change in core temperature upon acute cold exposure, indicating a role for FGF21 in maintainin

142 served an increase in BAT radio density upon cold exposure, indicating reduced BAT triglyceride conte

143 Indeed, acute cold exposure induced c-Fos (as a surrogate for neuronal

144 ons in vivo significantly attenuates chronic cold-exposure-induced alternative macrophage activation

145 long-term cold and epigenetically store this cold-exposure information to regulate flowering time.

146 We further showed that cold exposure inhibits atherosclerosis and improves endo

147 alterations in neurovascular function during cold exposure is clinically relevant.

148 The block to flowering prior to cold exposure is due to high levels of the flowering rep

149 Brown adipose tissue (BAT) activation via cold exposure is increasingly scrutinized as a potential

150 cute painful sensory neuropathy on sustained cold exposure is not yet known, but individuals of Afric

151 in response to physiologic stimuli, such as cold exposure, is controlled by its sympathetic innervat

152 ediates nonshivering thermogenesis and, upon cold exposure, is induced in brown adipose tissue (BAT)

153 d in the basal brain after either fasting or cold exposure, it was found that all activated neurons r

154 However, during cold exposure itself it is unknown whether vernalizing c

155 We show that cold exposure leads to marked shift of the microbiota co

156 Cold exposure led to downregulation of Ip6k1 in murine i

157 basal body temperature, improved response to cold exposure, lower plasma glucocorticoid levels, impro

158 a variable indoor environment with frequent cold exposures might be an acceptable and economic manne

159 mice neither alters energy expenditure upon cold exposure nor reduces browning in inguinal adipose t

160 RNA expression is dramatically elevated upon cold exposure of mice in both brown fat and skeletal mus

161 We then compared the influence of chronic cold exposure on noradrenergic modulation of the HPA str

162 a sensitizing stimulus, chronic intermittent cold exposure, on neuroendocrine and noradrenergic stres

163 nal intensity does not change in response to cold exposure or beta-adrenergic activation.

164 Cold exposure or beta-adrenergic stimulation favors the

165 white fat, is suppressed in mouse BAT during cold exposure or beta3-adrenergic stimulation, and is do

166 ocyte function in subcutaneous fat following cold exposure or beta3-agonist treatment.

167 in response to physiological stimuli such as cold exposure or exercise.

168 nvert to a "brown-like" state with prolonged cold exposure or exposure to beta-adrenergic compounds.

169 rison, insulin clearance was not affected by cold exposure or phentolamine infusion.

170 after stimulation of adrenergic signaling by cold exposure or treatment with a beta3-adrenergic agoni

171 ncreases in TPR in blacks than whites during cold exposure (P<0.05) but no group differences during h

172 n a murine model of LPS-induced peritonitis, cold exposure potentiated hypothermia and decreased surv

173 indicated that the racial differences during cold exposure probably reflected greater beta-adrenergic

174 ernalization, the process by which prolonged cold exposure provides competence to flower, is an impor

175 normal stimulation in BAT lipogenesis during cold exposure, rapidly exhausting the availability of fa

176 t, miR-155 mimics phenocopied the effects of cold exposure, reducing Ship1 and Socs1 and altering TNF

177 ot expressed in 50% of SCNx squirrels during cold exposure; rhythm amplitude was reduced to 25-40% of

178 In response to cold exposure, RYGB mice exhibited an improved capacity

179 BAT activity during 2 h of mild cold exposure served as a positive control experiment.

180 However, cold exposure shifted transcription to exon 1b, increasi

181 In contrast, mild cold exposure stimulates BAT energy expenditure with few

182 Cold exposure stimulates energy expenditure and glucose

183 In murine beige fat, cold exposure stimulates mitochondrial creatine kinase a

184 ing as erythematous plaques or nodules after cold exposure, that typically affects infants and childr

185 of anoxia-induced suspended animation before cold exposure, the associated cold-induced viability def

186 nt role in regulating heat production during cold exposure, the biological functions of UCP2 and UCP3

187 own adipose tissue (BAT) is activated during cold exposure to generate heat from nutrients.

188 Additionally, cold exposure up-regulates SIRT3 expression in brown fat

189 aratus and signal transduction, whereas upon cold exposure, up and down-regulated genes were similar

190 PDGFRalpha(+) cells and adipocytes prior to cold exposure, using Pdgfra-Cre recombinase estrogen rec

191 ensitivity of twitching to various levels of cold exposure was assessed in week-old rats that were un

192 using a murine model of local environmental cold exposure, we show that TRPA1 acts as a primary vasc

193 Enhancing energy expenditure by cold exposure will likely not impact obesity significant

194 tral nervous system (CNS) areas activated by cold exposure with brain regions anatomically linked to

195 play an impaired ability to adapt to chronic cold exposure, with diminished browning of WAT.