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1 was elevated and could account for sea otter hypermetabolism.
2 e hypometabolism as well as parietal glucose hypermetabolism.
3 8)F-FDG PET/CT showed limbic and extralimbic hypermetabolism.
4 hermogenic demand and is the source of basal hypermetabolism.
5 inant mitochondrial uncoupling syndrome with hypermetabolism.
6 y the focus of dysregulated inflammation and hypermetabolism.
7  regions with significant hypometabolism and hypermetabolism.
8 mal liver function, lipid abnormalities, and hypermetabolism.
9  glucose metabolism and amyloid-beta-related hypermetabolism.
10 creased browning of white adipose tissue and hypermetabolism.
11 l of malignant hyperthermia and heat-induced hypermetabolism.
12 at Abeta deposition directly caused reactive hypermetabolism.
13 s the dependable reversal of skeletal muscle hypermetabolism.
14 heral chemoreceptor gain is augmented during hypermetabolism.
15 entilation, was doubled during the period of hypermetabolism.
16 as recently been found to induce and sustain hypermetabolism.
17 urn long-term oxandrolone treatment improves hypermetabolism and body composition.
18         A severe burn injury leads to marked hypermetabolism and catabolism, which are associated wit
19                   Patients had corresponding hypermetabolism and cortical volume increase in the extr
20  study was to investigate activation-induced hypermetabolism and hyperemia by using a multifrequency
21  as being potentially associated with REE or hypermetabolism and hypometabolism after LTx.
22 s in accordance with the notion that glucose hypermetabolism and hypometabolism reflect fundamentally
23 th functional neuroimaging studies reporting hypermetabolism and increased regional cerebral blood fl
24                   In OHM1 and OHM2, relative hypermetabolism and interarterial watershed infarction o
25                                              Hypermetabolism and malnourishment are common in the int
26                         Burn trauma triggers hypermetabolism and muscle wasting via increased cellula
27 us in schizophrenia is characterized by both hypermetabolism and reduced size.
28 tabolic; TEE was not different in those with hypermetabolism and REE as a percentage of predicted was
29 ropranolol during hospitalization attenuates hypermetabolism and reverses muscle-protein catabolism.
30 the role of the inflammasome in burn-induced hypermetabolism and, potentially, developing novel thera
31 e and regional distribution of inflammation (hypermetabolism) and tissue failure, apoptosis, or atrop
32                            Because anorexia, hypermetabolism, and elevated cytokine levels are freque
33 hift towards glucose utilization, suppresses hypermetabolism, and reduces chemokine secretion and cel
34  body surface area), its effects on postburn hypermetabolism, and the long-term cosmetic and function
35 ngly associated with inflammatory signaling, hypermetabolism, and the senescence-associated secretory
36      FDG-PET demonstrated an area of intense hypermetabolism, and wide surgical resection was perform
37  of therapeutic strategies that aim to blunt hypermetabolism appears warranted.
38                         Sepsis and excessive hypermetabolism are also associated with protein catabol
39  cellular protection mechanisms and systemic hypermetabolism are initiated and controlled.
40                               Focal areas of hypermetabolism are noted occasionally, and the usual in
41                                              Hypermetabolism associated with severe burns was thought
42    The contralateral hemisphere did not show hypermetabolism at any time after ICH.
43                                          CA1 hypermetabolism at baseline predicted hippocampal atroph
44                                Focal glucose hypermetabolism at the level of cervical spinal cord com
45     The identification of unexpected foci of hypermetabolism at whole-body FDG PET may signal the pre
46  allows for accurate localization of foci of hypermetabolism based on 18FDG uptake in glycolytically
47 h scan was evaluated for abnormal unexpected hypermetabolism based on unusual location (ie, foci that
48 ignificantly associated with the presence of hypermetabolism before LTx and the cumulative dose of pr
49            Various conditions in which focal hypermetabolism can be encountered on (18)F-FDG PET stud
50 s regulate inflammatory cytokines that cause hypermetabolism/catabolism via acute phase response, lea
51 ism associated with putaminal and cerebellum hypermetabolism, compatible with encephalitis and especi
52  response contributes to multiorgan failure, hypermetabolism, complications, and death.
53 r, may contribute to multiple organ failure, hypermetabolism, complications, and death.
54 d resting energy expenditure, but if and how hypermetabolism contributes to disease pathology is unkn
55                                This regional hypermetabolism corresponds with mild neuroinflammation,
56 nd/or secondary effects such as hyperphagia, hypermetabolism, disturbed glucose homeostasis, altered
57              It has been recently shown that hypermetabolism does not completely resolve after healin
58 luid resuscitation, sepsis, immune function, hypermetabolism, early excision, wound healing, scar for
59 abolic balance (for example, weight loss and hypermetabolism) have been consistently shown to contrib
60 m were concomitant with a loss of lean mass, hypermetabolism, hepatic steatosis, dyslipidemia, and be
61                                              Hypermetabolism/hypometabolism were low but present at t
62 CT scans of 13 tumors showed intense diffuse hypermetabolism in 12 and response to therapy in all 12
63                         Our main finding was hypermetabolism in a cluster comprising the bed nucleus
64                                              Hypermetabolism in a ventral emotional neural system dur
65                                              Hypermetabolism in active UC colonoids is driven, in par
66 ectly the link between neuroinflammation and hypermetabolism in aged mice.
67 th the controversial observation of cerebral hypermetabolism in aging WT mice.
68 r previous finding of relative basal ganglia hypermetabolism in AIDS dementia complex (ADC) and to de
69 bolic disruptions, including weight loss and hypermetabolism in both patients and animal models.
70                                  The role of hypermetabolism in cancer cachexia remains unclear.We st
71 so shows that TSC patients with ASDs display hypermetabolism in deep cerebellar structures, compared
72 owed a nearly identical pattern of hypo- and hypermetabolism in groups 1 and 2.
73 flammation, consistent with prior reports of hypermetabolism in inflammatory disorders.
74                     Higher HOMA-IR predicted hypermetabolism in MCI-progressors and hypometabolism in
75 G uptake (regions with significant hypo- and hypermetabolism in patients with conversion vs. those wi
76  studies have revealed the presence of brain hypermetabolism in the brain stem and cervical spinal co
77                      In particular, abnormal hypermetabolism in the brain, as evaluated by(18)F-FDG P
78 tudies that have reported anterior cingulate hypermetabolism in the disorder.
79             Conversely, they showed relative hypermetabolism in the right inferior, middle, and super
80                             We also observed hypermetabolism in the same cluster in rats expressing c
81                                      Diffuse hypermetabolism in the subcortical and deep white matter
82 post hoc analyses, depressed patients showed hypermetabolism in these areas during both waking and NR
83                       Age-dependent cortical hypermetabolism in WT mice relative to young animals age
84 y; OR: 1.48 (95% CI: 1.01, 2.17); P = 0.044].Hypermetabolism is correlated with clinical and biologic
85                                  Conversely, hypermetabolism is likely compensatory in regions where
86                Studying the role of regional hypermetabolism is needed to better understand its inter
87 te; however, the tissue-level source of this hypermetabolism is unknown.
88 with decreased proinflammatory mediators and hypermetabolism, leading to a significant shorter ICU st
89         These findings show that hippocampal hypermetabolism leads to atrophy in psychotic disorder a
90                                         This hypermetabolism may be an adaptive response to an inabil
91                                              Hypermetabolism might be detrimental in other structures
92  suggest that the hyperpnoea observed during hypermetabolism might be mediated by an increase in the
93 cytokine expression profile, organ function, hypermetabolism, muscle protein synthesis, incidence of
94 ess response to burn trauma, with a focus on hypermetabolism, muscle wasting, and stress-induced diab
95 he human brain, (18)F-FDG PET shows cerebral hypermetabolism of aged wild-type (WT) mice relative to
96 f PAS kinase is consistent with the reported hypermetabolism of PAS kinase-deficient mice, identifyin
97  skeletal muscle may account for the resting hypermetabolism of patients with HIV lipoatrophy.
98 mal metabolic brain network characterized by hypermetabolism of the basal ganglia, supplementary moto
99 iscuss and illustrate the multiple causes of hypermetabolism on (18)F-FDG PET studies that should not
100                                              Hypermetabolism (P = 0.001) was revealed in the right su
101                                              Hypermetabolism (P = 0.001) was revealed in the right su
102                           We determined that hypermetabolism protected TAZ kd mice from weight gain.
103                                        While hypermetabolism remains an intriguing target for interve
104  process, but little is known about regional hypermetabolism, sometimes observed in the brain of pati
105  on (18)F-FDG PET studies include interictal hypermetabolism, Sturge-Weber syndrome, changes associat
106                 There were discrete areas of hypermetabolism suggestive of malignancy (positive) in 1
107                    Surprisingly, despite the hypermetabolism, their body temperature is not elevated.
108 valuate the intracranial lesions for glucose hypermetabolism to suggest malignancy, mutiplicity of in
109 tic patients, compared with normometabolism, hypermetabolism was associated with a reduced median sur
110  poor response to escitalopram, while insula hypermetabolism was associated with remission to escital
111 es were reported, although medulla oblongata hypermetabolism was associated with shortened survival (
112                                              Hypermetabolism was defined as REE > 110% of that predic
113                         In at-risk patients, hypermetabolism was found to begin in CA1 and spread to
114                                              Hypermetabolism was negatively correlated only with hypo
115                              The presence of hypermetabolism was significantly associated with the pr
116 The combination of frontal and parietal lobe hypermetabolism was uniquely found in CP-term cases.
117 imary lesion, 58 abnormal unexpected foci of hypermetabolism were identified in 53 patients.
118 ve blood loss, significant fluid shifts, and hypermetabolism, which alter the pharmacokinetics of man
119                        MH is associated with hypermetabolism, which has directed research interest in
120 ine reproduced a similar regional pattern of hypermetabolism, while repeated exposure shifted the hip
121 es showed a distinct combination of parietal hypermetabolism with cerebellar hypometabolism but intac
122 association between brain hypometabolism and hypermetabolism with motor scores of patients with early

 
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