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1 BAT also secreted several adipokines, including adiponec
2 BAT and beige fat oxidized fatty acids to fuel Ucp1-medi
3 BAT and the measurement of nasal sIgE can also contribut
4 BAT can also be used to monitor resolution of food aller
5 BAT dysfunction resulting from p62 deficiency is manifes
6 BAT functions as hepatoprotective machinery to counterac
7 BAT product was US-licensed in 2013.
8 BAT product was well tolerated in patients.
9 BAT results were assessed against confirmed allergic sta
10 BAT rPru p 3 and rMal d 3 were performed and sIgG4 antib
11 BAT using %CD63(+) basophils (SSClow/CCR3pos) as outcome
12 BAT volume and 18F-FDG uptake were not associated with q
13 BAT volume, BAT 18F-FDG uptake, and skeletal muscle 18F-
14 BAT was positive in 12 out of 15 patients and negative i
15 BAT was safe and significantly improved QOL, 6MHW, and N
16 BAT was safe and significantly improved QOL, exercise ca
17 BAT-specific deletion of Sirt5, a mitochondrial desuccin
18 BATs confirmed that, comparable to the anti-IgE monoclon
19 BATs to measure upregulation of basophil CD203c and indu
24 rmogenesis in humans; how to safely activate BAT and other organ thermogenesis; and how to sustain a
31 s tissue-cholesterol homeostasis and affects BAT metabolism, suggesting beneficial LAL activation in
35 lexaFFA uptake in the heart (48 +/- 20%) and BAT (40 +/- 10%) compared to saline-injected/fed mice.
36 BCN, only ratios of sIgG4/sIgE rMal d 3 and BAT rMal d 3 (0.001 ug/mL) can identify clinically relev
37 reased 3-hydroxybutyrate levels in blood and BAT in response to the cold, suggesting that ketogenesis
39 crease FFA uptake in the heart (fasting) and BAT [cold exposure and injection with the beta(3) adrene
46 nificant alterations in body temperature and BAT thermogenic gene expression, perhaps contributing to
48 revealed that BMAT is distinct from WAT and BAT, with altered glucose metabolism and decreased insul
53 we determined that transplantation of BAT (+BAT) improves cardiac function via the release of the li
56 We found ANKO mice, which lack NAMPT in both BAT and WAT, had impaired gene programs involved in ther
57 tabolism attenuates systemic BCAA clearance, BAT fuel oxidation and thermogenesis, leading to diet-in
59 bjects were randomized 1:1 to receive either BAT plus optimal medical management (BAT group) or optim
61 itoxin Heptavalent (A,B,C,D,E,F,G)-(Equine) (BAT) manufactured by Emergent BioSolutions Canada Inc is
62 sufficiency of UCP1 to account for eutherian BAT, these data support a mechanism for the emergence of
63 is the first, to our knowledge, to evaluate BAT in patients with melatonin deficiency (radiotherapy
71 Our results identify an endocrine role for BAT to enhance cardiac function that is mediated by regu
73 a promising approach to deriving functional BAT engraftment, which may be applied to therapeutic BAT
74 ANKO mice, which lack NAMPT in BAT only, had BAT cellular alterations similar to the ANKO mice, BANKO
78 CONCLUSIONThese findings indicate that human BAT metabolic activity can be increased after chronic ph
79 supraclavicular adipose tissue (where human BAT is localized) obtained from human subjects increased
82 ted sympathetic nerve activation and impairs BAT thermogenic programs, leading to reduced core body t
83 rgc1a promoter, which epigenetically impairs BAT thermogenesis and energy expenditure, predisposing o
89 fic deletion of the activin receptor ALK7 in BAT resulted in fasting-induced hypothermia due to exagg
90 ntrast, deletion of REV-ERBalpha and beta in BAT allowed mice to maintain their body temperature in c
91 abolism and body temperature and lower BW in BAT-Kiss1r KOs reveal a previously unidentified role for
92 Mechanistically, active BCAA catabolism in BAT is mediated by SLC25A44, which transports BCAAs into
97 thermogenesis and mitochondrial function in BAT and a blunted thermogenic (rectal temperature, BAT t
98 ring showed promoted thermogenic function in BAT and inguinal WAT through the upregulation of UCP1 an
99 th higher expression of thermogenic genes in BAT, and are protected from high-fat diet-induced obesit
100 n succinylation and malonylation are high in BAT and subject to physiological and genetic regulation.
103 Although BANKO mice, which lack NAMPT in BAT only, had BAT cellular alterations similar to the AN
104 ing the functional relevance of PHOPSPHO1 in BAT thermogenesis and energy metabolism, we show that PH
108 role for endogenous kisspeptin signaling in BAT in modulating metabolic and thermogenic physiology.
109 whether kisspeptin signaling specifically in BAT influences BW, metabolism, or body temperature, we u
111 tion of SREBP1 that drives fuel synthesis in BAT and is necessary to maintain circadian body temperat
112 eased markers of mitochondrial uncoupling in BAT suggest that BD-AcAc(2) initiates a transcriptional
113 innervating BAT, and dramatically increased BAT uncoupling protein 1 (Ucp1) expression and activity
114 ll four studied patients presented increased BAT volume and activity measured by positron emission to
116 ow that oral melatonin replacement increases BAT volume and activity and improves blood lipid levels
118 circuits and sympathetic nerves innervating BAT, and dramatically increased BAT uncoupling protein 1
122 ocnemius, subcutaneous WAT and interscapular BAT, coupled with neurochemical characterization of spec
123 2) silencing of the Pnpla2 in interscapular BAT causes a brown-to-white phenotypic shift accompanied
127 during cold stress in large mammals lacking BAT, strengthening the hypothesis that muscle NST has li
128 role in thermoregulation in species lacking BAT, we investigated the thermogenic capacities of newbo
129 ely test the premise that a thermogenic-like BAT phenotype is coupled with enhanced glucose tolerance
130 se findings indicate that a thermogenic-like BAT phenotype is not linked to heightened glucose tolera
131 either BAT plus optimal medical management (BAT group) or optimal medical management alone (control
132 in stimulates a hypothalamus-adrenal medulla-BAT axis, which is necessary and sufficient to induce li
135 ed KLF15 and POX expression levels in mutant BAT, suggesting that loss of BAT ALK7 results in excessi
138 ized brain alcohol-sensing/sympathetic nerve/BAT/liver axis that counteracts liver steatosis and inju
142 duced by adrenergic stimulation of NCLX-null BAT, triggers the mitochondrial permeability transition
145 at thermoneutrality, enhanced activation of BAT and its thermogenic phenotype via chronic mild cold
147 am of ALK7 which regulates the adaptation of BAT to nutrient availability by limiting nutrient stress
148 We aimed to investigate the associations of BAT volume and 18F-fluordeoxyglucose (18F-FDG) uptake af
150 gnificantly enhanced thermogenic capacity of BAT, and this effect was diminished in Opn3-KO animals.
152 s is currently impeded by poor efficiency of BAT tissue formation in vivo and undesirably short engra
154 ata support a mechanism for the emergence of BAT based on the acquisition of a novel capacity for adi
155 g of this event relative to the emergence of BAT, the phylogeny of CHKB-CPT1B synteny, and the insuff
156 Therefore, in the further exploration of BAT as a potential source of novel drug targets, we disc
158 evels in mutant BAT, suggesting that loss of BAT ALK7 results in excessive activation of glucocortico
161 we discuss the hypothalamic orchestration of BAT activity and the relatively unexplored BAT feedback
164 gion, which co-locates to the main region of BAT in adult humans, and is indicative of thermogenesis.
165 r data identify p62 as a master regulator of BAT function in that it controls the Ucp1 pathway throug
166 role of PHOSPHO1 as a negative regulator of BAT thermogenesis, and inhibition of PHOSPHO1 or enhance
168 Here, we show that adrenergic stimulation of BAT activates a PKA-dependent mitochondrial Ca(2+) extru
169 e elapsed after meal consumption nor that of BAT 18F-FDG uptake x time elapsed after meal consumption
170 Here, we determined that transplantation of BAT (+BAT) improves cardiac function via the release of
172 brown progenitor cells sorted from offspring BAT demonstrated attenuated brown adipogenic capacity.
174 tures that may provide useful information on BAT, the impact of reconstruction methods and imaging mo
184 esults demonstrate that caffeine can promote BAT function at thermoneutrality and may have the potent
185 T/CT appear to provide information regarding BAT activity distinct from SUV(max) These features might
186 nce of BAT/BAT-like tissue in humans renders BAT as an attractive target against obesity and insulin
187 usion: Several clusters of highly repeatable BAT radiomic features derived from (18)F-FDG PET/CT appe
188 nction of UCP1 and other proteins in Sirt5KO BAT results in impaired mitochondria respiration, defect
189 nravel an unrecognized LepR neuron Sh2b1/SNS/BAT/thermogenesis axis that combats obesity and metaboli
190 mediobasal hypothalamus also impairs the SNS/BAT/thermogenesis axis; conversely, hypothalamic overexp
192 tion during cold exposure acutely suppresses BAT temperature in wild-type mice but not in Opn5-null m
196 d a blunted thermogenic (rectal temperature, BAT temperature, and whole-body oxygen consumption) resp
197 though UCP1 expression declined in long-term BAT grafts, this deterioration can be reversed by swimmi
199 c performance of a basophil activation test (BAT) and sIgG4 in nsLTP-sensitized patients from Antwerp
200 administering the basophil activation test (BAT) and the skin prick test (SPT) and measuring the lev
201 in vivo tests and basophil activation test (BAT) for the diagnosis of IHRs due to metronidazole and
204 (according to the basophil activation test [BAT]) might meet this requirement for different IgE-depe
215 : a mononucleotide (A) microsatellite at the BAT-26 locus and a dinucleotide (CA) microsatellite in t
216 ian preoptic area (MnPO) neurons blocked the BAT thermogenic responses during both PGE(2)-induced fev
221 so-called nondiagnostic applications of the BAT involve therapeutic monitoring, follow-up of natural
222 Determination of whether modulation of the BAT morphology/function drives changes in glucoregulatio
223 lso become clear that appropriate use of the BAT necessitates knowledge about degranulation metrics a
224 cell cycle, and the further expansion of the BAT was mainly due to lipogenesis-mediated BAs volume in
226 that, following adrenergic stimulation, the BAT temperature of knockout mice increases more and fast
227 viously defined optimal cutoff was used, the BAT diagnosed PA with 98% specificity and 75% sensitivit
228 n 100% of SAR and group A cases, whereas the BAT with perennial allergens was positive in 37.5% and 6
230 ectiveness of baroreflex activation therapy (BAT) in patients with heart failure with reduced ejectio
231 ruxolitinib (RUX) to best available therapy (BAT) in HC-RES/INT ET, which showed no difference betwee
234 mportance of brown and white adipose tissue (BAT and WAT) NAD(+) metabolism in regulating whole-body
235 hat, on cold exposure, brown adipose tissue (BAT) actively utilizes BCAA in the mitochondria for ther
236 hly enriched in mature brown adipose tissue (BAT) and is further induced by cold and isoproterenol tr
237 ipose tissue (WAT) and brown adipose tissue (BAT) are involved in whole-body energy homeostasis and m
238 n (placental) mammals, brown adipose tissue (BAT) can also dissipate this proton gradient through unc
240 ma is that thermogenic brown adipose tissue (BAT) contributes to improvements in glucose homeostasis
241 rticoids (GC) on fetal brown adipose tissue (BAT) development and its long-term thermogenesis and ene
244 tent, energy-consuming brown adipose tissue (BAT) in adult humans, much effort has been devoted to ex
246 However, the role of brown adipose tissue (BAT) in regulating gestational metabolism is unknown.
247 ences thermogenesis of brown adipose tissue (BAT) independent of ambient temperature conditions.
259 es muscle hypertrophy, brown adipose tissue (BAT) thermogenesis, and white adipose tissue (WAT) lipol
260 cused on its effect on brown adipose tissue (BAT) thermogenesis, though its effect on browning of whi
261 disease by increasing brown adipose tissue (BAT) thermogenesis, white adipose tissue (WAT) lipolysis
262 arks the activation of brown adipose tissue (BAT) thermogenesis, yet the mechanisms preventing Ca(2+)
266 WAT) and interscapular brown adipose tissue (BAT) to an acute (48 h) cold stress or challenge with th
267 ly, direct exposure of brown adipose tissue (BAT) to light in living mice significantly enhanced ther
268 late the adaptation of brown adipose tissue (BAT), a key organ for non-shivering thermogenesis, to va
269 lic tissues, including brown adipose tissue (BAT), but it is unknown which specific tissue is respons
270 energic stimulation of brown adipose tissue (BAT), p38 phosphorylates the activating transcription fa
271 such as the heart and brown adipose tissue (BAT), where substrate preference changes in pathophysiol
282 eries relative to the glutamatergic drive to BAT sympathoexcitatory neurons in DMH augment our unders
283 urther show that Opn5 POA neurons project to BAT and decrease its activity under chemogenetic stimula
285 erforation following blunt abdominal trauma (BAT) is an uncommon situation with high morbidity and mo
297 a transcriptional signature consistent with BAT thermogenesis in the context of HFD-induced obesity.
298 diomic feature repeatability correlates with BAT SUV(max) repeatability, participants were stratified