ライフサイエンスコーパス: cold exposure

1 ients with type 2 diabetes during controlled cold exposure.

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

3 AgRP neurons in the hyperphagic response to cold exposure.

4 creates a partially vernalized state without cold exposure.

5 tered in brown adipose tissue in response to cold exposure.

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

7 alpine habitats must retreat to avoid lethal cold exposure.

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

9 rates transcriptional shutdown of FLC during cold exposure.

10 ynthesis and prevent oxidative damage during cold exposure.

11 otect their core temperatures in response to cold exposure.

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

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

14 s they aged and developed hypothermia during cold exposure.

15 yed substantial NEFA and glucose uptake upon cold exposure.

16 cts to the DMH and expresses c-Fos following cold exposure.

17 itter release to brown adipose tissue during cold exposure.

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

19 roteins after salt exposure when compared to cold exposure.

20 diture increased to similar levels as during cold exposure.

21 l for appropriate thermogenic response after cold exposure.

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

23 2.2, relative to start-of-century population cold exposure.

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

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

26 r pharmacological beta-adrenergic agonism or cold exposure.

27 450 h CR) trees under controlled-environment cold exposure.

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

29 luding reduced ATP levels and intolerance to cold exposure.

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

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

32 e is reduced and remains unchanged following cold exposure.

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

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

35 and formed less multilocular structures upon cold exposure.

36 ng sympathetic premotor neurons activated by cold exposure.

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

38 d for de novo beige fat biogenesis following cold exposure.

39 ratios and provides metabolic savings during cold exposure.

40 athione peroxidase expression increased with cold exposure.

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

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

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

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

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

46 por nearly continuously throughout 2.5 yr of cold exposure.

47 ed during the initial rewarming period after cold exposure.

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

49 nalysis to identify cDNAs rapidly induced by cold exposure.

50 s were monitored during moderate and extreme cold exposure.

51 T/CT imaging was performed immediately after cold exposure.

52 bitum EI increased during but not after mild cold exposure.

53 ith increased vulnerability to environmental cold exposure.

54 vulnerable to lethal hypothermia under acute cold exposure.

55 ith changes in ad libitum EI during or after cold exposure.

56 87 kcal/d, P = 0.006), but not the day after cold exposure.

57 ce had preserved core body temperature after cold exposure.

58 ttenuated core-temperature drop during acute cold exposure.

59 nces in adipocyte populations with aging and cold exposure.

60 own adipose tissue (BAT) and is induced upon cold exposure.

61 r = 0.33, P = 0.02), but not with EI during cold exposure.

62 in metabolism, primarily induced by chronic cold exposure.

63 nd also displayed cold sensitivity following cold exposure.

64 of wheals, angioedema or both in response to cold exposure.

65 sponses during both PGE(2)-induced fever and cold exposure.

66 in circadian body temperature during chronic cold exposure.

67 and Ffg21 mRNA expression in iWAT following cold exposure.

68 inguinal white adipose tissue after chronic cold exposure.

69 ic metabolism in adipose depots during acute cold exposure.

70 strate the distinct metabolism of BAT during cold exposure.

71 ases disproportionately during environmental cold exposure.

72 me severely hypothermic and succumb to acute cold exposure.

73 ergo specific metabolic changes during acute cold exposure.

74 eserve glucose homeostasis in the setting of cold exposure.

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

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

77 rature compared to UCP1KO alone during acute cold exposure.

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

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

80 vere defect in BAT oxidative metabolism upon cold exposure.

81 35-37 degrees C) during the entire period of cold exposure.

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

83 Here we show that during chronic cold exposure (1 wk at 4 degrees C), genes controlling d

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

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

86 ithin the SCV region after 1 h of whole-body cold exposure (18 degrees C), using MRI in 26 boys aged

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

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

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

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

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

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

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

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

95 Long-term cold exposure (5th vs 50th percentile of mean temperatur

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

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

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

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

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

101 During cold exposure, activated brown adipose tissue (BAT) take

102 Cold exposure acutely increases Afadin protein levels an

103 Moreover, violet photostimulation during cold exposure acutely suppresses BAT temperature in wild

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

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

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

107 Cold exposure also increased blood pressure and energy e

108 Cold exposure also produced mechanical hyperalgesia as m

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

110 ironment, including high-altitude, heat, and cold exposure, alters nutrition requirements have been s

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

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

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

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

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

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

117 Ex vivo fluorescence imaging after overnight cold exposure and fasting produced a significant increas

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

119 ve that it is further altered in response to cold exposure and highlight myosin as a potentially cont

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

121 e FFA uptake in the heart (fasting) and BAT [cold exposure and injection with the beta(3) adrenergic

122 erived FGF21 enters circulation during acute cold exposure and is critical for thermoregulation.

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

124 esis and dysregulates adipocyte responses to cold exposure and provides a resource for identifying co

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

126 during brown fat cell differentiation and by cold exposure and that Dot1l and its H3K79 methyltransfe

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

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

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

130 fat by agents that modulate cAMP levels, by cold exposure, and by pharmacological stimulation of bet

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

132 dria contacts change in response to fasting, cold exposure, and exercise.

133 ata, with regional differentiation following cold exposure, and expression shifts invariant among pop

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

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

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

137 ity and the genes suppressed after 7 days of cold exposure are enriched in photosynthesis-associated

138 experimental settings, and triggers such as cold exposure are known to precipitate vaso-occlusive cr

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

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

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

142 neuron activation occurs rapidly upon acute cold exposure, as do increases of both energy expenditur

143 its proteolysis is inhibited in response to cold exposure, as its function requires concomitant cold

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

145 Here we report that, on cold exposure, brown adipose tissue (BAT) actively utili

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

147 he physiological site of FGF21 action during cold exposure by impairing FGF21 signaling to adipose ti

148 ace-targeting protein in adipose tissue upon cold exposure by liquid chromatography-tandem mass spect

149 Cold exposure can enhance energy expenditure by activati

150 Acute heat and cold exposure can increase or decrease the risk of morta

151 ic response of white adipose tissue (WAT) to cold exposure (CE) in mice, exploring the cross talk bet

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

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

154 As the thermogenic response to mild cold exposure (COLD) may similarly characterize this hum

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

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

157 After 3 days of cold exposure, core body temperature was significantly r

158 Cold exposure decreased p53 in beiging WAT of young mice

159 (2.42 +/- 0.85 vs. 3.43 +/- 0.93, P = 0.02), cold exposure decreased the (11)C-HED RI in WAT (0.44 +/

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

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

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

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

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

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

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

167 Additionally, cold exposure elevates SIRT2 expression in brown adipose

168 hese data suggest that in healthy young men, cold exposure elicits a dynamic and heterogeneous respon

169 Cold exposure facilitates the selective packaging of miR

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

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

172 t, highlighting the importance of sufficient cold exposure for flowering, fruiting, and ripening.

173 altered by aerobic exercise, starvation, and cold exposure, for example, there appears to be coordina

174 In this cohort study, long-term heat and cold exposure from the second trimester until 4 weeks af

175 Acute cold exposure further augmented B-adrenergic signaling i

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

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

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

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

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

181 tial changes in population-weighted heat and cold exposure in 47 US metropolitan regions during the 2

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

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

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

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

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

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

188 Acute cold exposure in mature animals augments BAT thermogenes

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

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

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

192 Cold exposure in normoxia or hypoxia increased mitochond

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

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

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

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

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

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

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

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

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

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

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

204 ockout mice accumulate acylcarnitines during cold exposure, indicating defective fatty acid oxidation

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

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

207 Cold exposure induced cAMP-dependent protein kinase-depe

208 Cold exposure induced more vaso-occlusion in nonhyperalg

209 In this regard, cold exposure induced the delayed appearance of multiple

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

211 ominated by pro-inflammatory M1 macrophages; cold exposure induces an M1-to-M2 shift in macrophage co

212 We show that cold exposure induces temperature-specific changes to th

213 In brown adipose tissue (BAT), short-term cold exposure induces the activating transcription facto

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

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

216 ), an alternative homeostatic state in which cold exposure inhibits thermogenesis and warm exposure s

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

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

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

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

221 Cold exposure is one of the options to activate brown ad

222 Additionally, end-of-century population cold exposure is projected to rise by a factor of 1.3-2.

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

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

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

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

227 the mode of beige adipocyte biogenesis upon cold exposure later in life.

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

229 Cold exposure led to downregulation of Ip6k1 in murine i

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

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

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

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

234 Here we show that cold exposure of obese mice triggers an adaptive tissue

235 lipid metabolism, but the impact of chronic cold exposure on circadian lipid metabolism in thermogen

236 We additionally evaluated the effects of cold exposure on H. halys adult longevity and fecundity.

237 nsidered the effect of different duration of cold exposure on mortality.

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

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

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

241 Cold exposure or beta-adrenergic stimulation favors the

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

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

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

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

246 During chronic cold exposure or ISR activation, Them1 accumulated in th

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

248 ding protein (ChREBP) in response to chronic cold exposure or to the activation of the integrated str

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

250 Cold exposure or treatment with B-adrenergic receptor ag

251 stress, such as during prolonged fasting or cold exposure, organisms need to balance the feeding of

252 During cold exposure over the first 5 days of life, total heat

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

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

255 Here, we show that cold exposure predominantly increases the expressions of

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

257 e-body oxygen consumption) response to acute cold exposure, prolonged fasting, and administration of

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

259 with greater ad libitum EI on the day after cold exposure (r = 0.29, P = 0.049 and r = 0.33, P = 0.0

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

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

262 Mechanistically, cold exposure repressed autophagy in beiging WAT of youn

263 intain body temperature in response to acute cold exposure require histone deacetylase 3 (HDAC3).

264 DHA was not able to counteract the impaired cold exposure response in BAT of obese-aged mice.

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

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

267 ents; animal contact; environmental heat and cold exposure; self-harm; and executions and police conf

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

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

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

271 Cold exposure stimulates energy expenditure and glucose

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

273 Prolonged cold exposure stimulates the formation of brownlike adip

274 Prolonged cold exposure stimulates the recruitment of beige adipoc

275 es (FGF21 AdipoKO), we performed a series of cold exposure studies to examine the tissue specific ind

276 btained from human subjects increased during cold exposure, suggesting our finding in rodents could a

277 ely, activation of BAT and beige fat through cold exposure suppressed alcoholic liver disease develop

278 dergoes a dynamic, heterogeneous response to cold exposure that can include the simultaneous synthesi

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

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

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

282 To maintain energy homeostasis during cold exposure, the increased energy demands of thermogen

283 Cold exposure then changes the chromatin by reducing nuc

284 isomal biogenesis was induced in response to cold exposure through activation of the thermogenic core

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

286 gRP neurons selectively blocks the effect of cold exposure to increase food intake but has no effect

287 Cold exposure triggers neogenesis in classic interscapul

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

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

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

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

292 e induction of thermogenic markers following cold exposure was reduced, but the effect was less prono

293 the emergence of uncoupling protein 1 after cold exposure was restricted to a subpopulation of MCT1-

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

295 , greater increases in RER and CARBOX during cold exposure were associated with greater ad libitum EI

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

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

298 lucose (18F-FDG) uptake after a personalized cold exposure with energy intake and appetite-related se

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

300 intain body temperature in response to acute cold exposure without food and become hypothermic within