ライフサイエンスコーパス: cerebral metabolism

1 er than voluntary exercise through increased cerebral metabolism.

2 quantify cerebral autoregulation as well as cerebral metabolism.

3 onic acid (AMPA) receptors to the control of cerebral metabolism.

4 d MRS) are able to assess both perfusion and cerebral metabolism.

5 of 'isolated' mitochondrial failure on local cerebral metabolism.

6 nclear how mitochondrial dysfunction affects cerebral metabolism.

7 that may reflect compensatory alterations in cerebral metabolism.

8 hat glucocorticoids have a central action on cerebral metabolism.

9 18F]-2-fluoro-2-deoxy-D-glucose to determine cerebral metabolism.

10 ocampal volume, brain amyloid deposition and cerebral metabolism.

11 Among the various techniques used to study cerebral metabolism, (13)C magnetic resonance spectrosco

12 etween re-establishment of apparently normal cerebral metabolism after HI, and the start of secondary

13 posed approach using PET to examine regional cerebral metabolism and look for characteristic patterns

14 evious work had shown a relationship between cerebral metabolism and NMDA receptor activity.

15 conducted with fluorodeoxyglucose to measure cerebral metabolism and Pittsburgh compound B for fibril

16 ion of the effects of general anesthetics on cerebral metabolism as revealed by imaging for therapeut

17 One possibility is that lifetime cerebral metabolism associated with regionally specific

18 The return to baseline of CBF and cerebral metabolism at normocapnia seen in our study wit

19 stages of Alzheimer's disease despite normal cerebral metabolism at rest.

20 dent effects of hyperglycemia and ketosis on cerebral metabolism, blood flow, and water distribution.

21 uronal firing patterns, neuromodulators, and cerebral metabolism change across sleep-waking states, a

22 Abnormal patterns of cerebral metabolism during non-REM sleep in depressed pa

23 slow waves to reduced neuronal activity and cerebral metabolism during partial seizures, but found i

24 Abnormalities in cerebral metabolism during stimulation appeared in the f

25 repsilon4 was also associated with decreased cerebral metabolism, especially in right middle frontal

26 rameters (systemic blood pressure, anaerobic cerebral metabolism, excessive brain tissue oxygenation,

27 c magnetic resonance imaging and on regional cerebral metabolism for glucose by positron emission tom

28 In order to measure the extent of cerebral metabolism in animals with different exercise r

29 The variations in cerebral metabolism in chronic PVS patients indicate tha

30 ermine the effect of normobaric hyperoxia on cerebral metabolism in patients with severe traumatic br

31 effects of chronic haloperidol treatment on cerebral metabolism in schizophrenic patients, 2) the re

32 yglucose (FDG) were used to measure regional cerebral metabolism in seven schizophrenic patients judg

33 ctual ability were inversely correlated with cerebral metabolism in the prefrontal, pre-motor, and le

34 on-PDD), compared with controls, had reduced cerebral metabolism in the primary occipital cortex (BA

35 went positron emission tomography to measure cerebral metabolism in this cross-sectional study.

36 saline-treated animals, the lesion increased cerebral metabolism in typical basal ganglia regions, su

37 ises to be a useful method for investigating cerebral metabolism in vivo.

38 tter study also found significantly improved cerebral metabolism (in 3 of 6 cortical and 3 of 7 subco

39 T images of AD demonstrate focally decreased cerebral metabolism involving especially the posterior c

40 Previous imaging studies have shown that cerebral metabolism is gradually reduced at the beginnin

41 These data demonstrate that cerebral metabolism is significantly compromised during

42 the beneficial effects of FPSA treatment on cerebral metabolism more precisely and rapidly than ICP

43 nsgenic mice, the results suggest that local cerebral metabolism of beta-amyloid precursor protein ma

44 The effects of the cerebral metabolism of the high levels of ammonia that c

45 In addition, baseline cerebral metabolism (PCr/NTP) may identify vulnerable in

46 ential for in vivo non-invasive detection of cerebral metabolism post-TBI, providing a new tool to mo

47 ower blood flow velocity, indicating reduced cerebral metabolism, predicted depressive symptoms and d

48 approximately 60-70% maximal oxygen uptake, cerebral metabolism remains elevated but perfusion in th

49 This study further determined the changes in cerebral metabolism resulting from the two methods of ex

50 General anesthetics suppress cerebral metabolism significantly.

51 Reductions in cerebral metabolism sufficient to impair cognition in no

52 and demonstrated marked decreases in overall cerebral metabolism to 30-40% of normal.

53 (PiB) positron emission tomography (PET) and cerebral metabolism using [(18)F]fluoro-2-deoxy-d-glucos

54 Cerebral metabolism was affected bilaterally in a subset

55 hourly by a parenchymal Clark electrode, and cerebral metabolism was assessed by the lactate/pyruvate

56 Non-oxidative cerebral metabolism was calculated from the ratio of oxy

57 Furthermore, cerebral metabolism was depressed significantly in a tim

58 Cerebral metabolism was determined in 35 brain structure

59 he same divers, the impact of hypercapnia on cerebral metabolism was determined using varying levels

60 omplaint was progressive dysfluency, resting cerebral metabolism was measured using [18F]fluorodeoxyg

61 rval, 0.06-0.16), and the initial pattern of cerebral metabolism was significantly associated with th

62 Local rates of cerebral metabolism were determined after an intravenous

63 Furthermore, decreases in cerebral metabolism were more intense and widespread.