ライフサイエンスコーパス: hyperperfusion

1 e interval 0.4% to 2.6%]) patients developed hyperperfusion.

2 and thalamus without cortical or cerebellar hyperperfusion.

3 ing patients vulnerable to cerebral hypo- or hyperperfusion.

4 xic edema, partial contrast enhancement, and hyperperfusion.

5 n after donor nephrectomy is attributable to hyperperfusion and hypertrophy of the remaining glomerul

6 nce, etiology, and prevention strategies for hyperperfusion and ICH following CAS.

7 The correspondence between the detected hyperperfusion and the postoperative resection cavity or

8 the ability of these endpoints to detect HCC hyperperfusion and, thereby, evaluated the suitability i

9 phy protocol; it finds relevantly more ictal hyperperfusion, and halves the radiation dose in about h

10 Although interictal hypoperfusion and ictal hyperperfusion are established localizing findings in pa

11 scular instability and cerebral ischemia and hyperperfusion are high, and anesthesia management shoul

12 Regions with ictal hyperperfusion are suggested to reflect seizure onset an

13 Identifying this pattern of hyperperfusion as typical for mesial temporal onset seiz

14 btractions were segmented to show regions of hyperperfusion at 1 SD above the mean.

15 ectomy (PH) in patients is leading to portal hyperperfusion but reduced hepatic arterial perfusion (H

16 In LT, portal hyperperfusion can severely impair graft function and su

17 the ictal studies, and three showed regional hyperperfusion corresponding to the hyperperfused region

18 usion" (CPP<CPPopt), severe disability with "hyperperfusion" (CPP>CPPopt), and favorable outcome was

19 Moreover, hyperperfusion did not correct the abnormal bioenergetic

20 ted as positive for osteomyelitis when focal hyperperfusion, focal hyperemia and focal bony uptake on

21 e same risk factors are involved in cerebral hyperperfusion following carotid endarterectomy.

22 Indeed, within 3 months after symptom onset, hyperperfusion had a positive predictive value of 88% fo

23 conclusion, diazepam normalized hippocampal hyperperfusion in CHR-P individuals, consistent with evi

24 EG) monitored interictal SPECT (IISPECT) and hyperperfusion in immediate postictal or periictal SPECT

25 Regional cerebral hyperperfusion in individuals at increased risk of AD in

26 ly (P = 0.11) so; (b) the lower incidence of hyperperfusion in PISPECT in our series was due to the o

27 ess often concordant with the EEG focus than hyperperfusion in PISPECT, but not significantly (P = 0.

28 , AA showed increased grey matter volume and hyperperfusion in right posterior neocortical areas impl

29 ocalized MTLE most commonly show a region of hyperperfusion in the anterior temporal region, which of

30 uring typical gelastic seizures demonstrated hyperperfusion in the hamartomas, hypothalamic region, a

31 erfusion that corresponded to the regions of hyperperfusion in the ictal studies, and three showed re

32 emission computed tomography revealed focal hyperperfusion in the region of the cerebellar mass.

33 or periictal aphasia, SPECT imaging revealed hyperperfusion in the speech cortex lacking sEEG coverag

34 "Hyperperfusion index (HPi)," defined as posttransplant p

35 were measured under basal conditions, during hyperperfusion induced by pharmacological vasodilation w

36 sing HAP need to be evaluated to reverse the hyperperfusion-induced impairment of the spontaneous cou

37 Portal hyperperfusion is frequently associated with early allog

38 Significant hyperperfusion is uncommon, even at a time when conventi

39 Results: Ictal hyperperfusion maps partially overlapped concomitant sEE

40 ion (n = 1) or hypoperfusion with peripheral hyperperfusion (n = 1) in the area of stroke, hypoperfus

41 NF), air trapping/hypoperfusion (AT), normal/hyperperfusion (NOR), and bulla/cysts (BUL).

42 s, severe ventilation-perfusion mismatch, or hyperperfusion of nonoxygenated regions.

43 he resting-state functional connectivity and hyperperfusion of pain processing areas of the brain hav

44 We aimed to identify factors associated with hyperperfusion-related graft injury and develop a predic

45 cardiac arrhythmic death and one death from hyperperfusion-related intracerebral hemorrhage.

46 Cerebral hyperperfusion syndrome (CHS) is an important complicati

47 Hyperperfusion syndrome and ICH can complicate carotid r

48 The study defined the incidence of cerebral hyperperfusion syndrome and intracranial hemorrhage (ICH

49 epartment to identify patients who developed hyperperfusion syndrome and/or ICH.

50 The hyperperfusion syndrome occurs infrequently following CA

51 attern of interictal hypoperfusion and ictal hyperperfusion that has been observed in subjects with e

52 ean rCBV, mean leakage coefficient K(2), and hyperperfusion volume (HPV), which is the fraction of th

53 Regional hyperperfusion was found in APOE epsilon4+group (left ci

54 ts in participants with ASD in regions where hyperperfusion was greatest.

55 The presence of hyperperfusion was inversely related to the occurrence o

56 Contralateral cerebellar hyperperfusion was observed in all cases.

57 This hyperperfusion was quantified by measuring the fraction

58 The most-contiguous area of hyperperfusion was the anterior temporal area extending

59 d quantitative FMT signal, denoting synovial hyperperfusion, was used to differentiate between synovi

60 We observed intense hyperperfusion within and at the edge of progressive mul