ライフサイエンスコーパス: central vein

1 ng the sinusoid from the portal triad to the central vein.

2 portal region of the liver lobule toward the central vein.

3 e left ventricle cavity or more simply via a central vein.

4 single layer of hepatocytes surrounding the central vein.

5 r systemic anticancer treatment (SACT) via a central vein.

6 e subset of hepatocytes most adjacent to the central veins.

7 e clinical data, for the presence of visible central veins.

8 67 years) who underwent MR venography of the central veins.

9 n 1-2 cell layers of hepatocytes surrounding central veins.

10 stricted to a layer of cells surrounding the central veins.

11 all hepatocytes except those encircling the central veins.

12 atic parenchyma and around portal tracts and central veins.

13 mmune cells infiltrate around the portal and central veins.

14 ssociated liver disease, progressive loss of central vein access, and repeated life-threatening centr

15 ifferent metabolic processes surrounding the central vein and its relation to liver homeostasis and d

16 n disease and dementia with Lewy bodies, the central vein and peripheral rim signs in multiple sclero

17 region of the hepatic lobule surrounding the central vein and regulates multiple functions of this re

18 ocesses, such as leptomeningeal involvement, central vein and rim of lesions, microstructural abnorma

19 he outward growth of MS lesions around their central vein and suggests that factors mediating lesion

20 protein was located around the liver lobule central vein and was low in CTR fetuses but rose to 63%

21 xytol-enhanced MR venography of the thoracic central veins and conventional venography within 6 month

22 panied moderately to markedly dilated portal/central veins and endothelialitis disproportionate to th

23 ngs of moderately to markedly dilated portal/central veins and endothelialitis disproportionate to th

24 8 hours, 57% +/- 1% portal areas, 40% +/- 1% central veins, and a few sinsusoidal cells expressed TNF

25 e kinases was detected preferentially in the central vein area, resulting in an atypical enrichment o

26 recruitment of hepatocytes upstream from the central vein area.

27 econstruction images were used to categorize central veins as patent, occluded, or narrowed.

28 mice demonstrated dilatation of the hepatic central vein at baseline and postinfection, compared wit

29 efore PH; in 76% +/- 3% portal areas and 75% central veins at 1 hour; and in 88% +/- 2% portal areas

30 nd in 88% +/- 2% portal areas and 80% +/- 9% central veins at 48 hours after PH.

31 ication depends on amino acid infusion via a central vein because of the immature gastrointestinal tr

32 08 who completed the follow-up period of the Central Vein Bypass Study.

33 I, 1.83-6.00; p = 0.044), and retention of a central vein catheter (AOR, 4.85; 95% CI, 2.54-9.29; p =

34 , 2.15-19.79; p = 0.004), and retention of a central vein catheter (AOR, 6.21; 95% CI, 3.02-12.77; p

35 g patients who initiated hemodialysis with a central vein catheter (CVC), a strategy that maximized A

36 culture every 7 days, and (4) pooling of all central vein catheter lumens in 1 blood culture bottle.

37 ification of treatment-related risk factors: central vein catheter retention, inadequate initial fluc

38 ment-related factors, including retention of central vein catheters and inadequate initial fluconazol

39 of initial antifungal therapy and removal of central vein catheters may improve the outcomes of patie

40 Among 1,419 patients (3,275 arterial or central-vein catheters) included, we identified 296 colo

41 ped fatty liver, necrosis, inflammation, and central vein collagen deposition.

42 hepatic arteries, portal veins, and hepatic central veins, consistent with its known vascular distri

43 hat necrosis begins adjacent to the lobule's central vein (CV) and progresses outward.

44 In current literature central vein disease (CVD) is defined as at least 50% na

45 ated that the hepatocellular parenchymal and central vein doses could be at significant levels becaus

46 expression occurring along portal tract and central vein endothelia and scattered bile duct epitheli

47 r sinusoidal lining cells, portal tract, and central vein endothelia.

48 SH, suggesting profibrotic crosstalk between central vein endothelial and hepatic stellate cells with

49 D133(+)/CD45(+) progenitors replace SECs and central vein endothelial cells after injury.

50 Adjacent central vein endothelial cells provide Wnt signals that

51 ile central vein hepatocytes were decreased, central vein endothelial cells were expanded.

52 CD133(+)/CD45(+) progenitors also repaired central vein endothelium.

53 cated that only a few hepatocytes around the central vein expressed viral surface antigen (HBsAg) in

54 xpression in hepatocytes in proximity to the central vein functionally defining zone 3 of the liver l

55 ession was detected in those adjacent to the central vein, gradually decreasing towards the portal tr

56 WNT2, important in central vein hepatocyte development, was down in sAH, wh

57 Interestingly, while central vein hepatocytes were decreased, central vein en

58 NCE Viral biosynthesis is highest around the central vein in the hepatitis B virus (HBV) transgenic m

59 ting and self-renewing cells adjacent to the central vein in the liver lobule.

60 secreted ST6Gal1 is produced by cells lining central veins in the liver and that IgG sialylation is p

61 rehensive evaluation of abnormalities of the central veins in the thorax, particularly with regard to

62 Surviving progenitors associate mainly with central veins, in a pattern of selection different from

63 collagen extended from the portal tracts and central veins into the parenchyma of about one quarter o

64 ion in the branch vein occlusion (BRAVO) and central vein occlusion (CRUISE) trials.

65 We found an increased incidence of central vein occlusion and elevated intraocular pressure

66 The results of the Central Vein Occlusion Study (CVOS) guide the management

67 The results of the Central Vein Occlusion Study guide the management of com

68 The Collaborative Central Vein Occlusion Study randomized trial of laser p

69 information on the early natural history of central vein occlusion that includes a 16% conversion of

70 in thickness of the most affected quadrant (central vein occlusion) or hemisphere (branch vein occlu

71 icularly intense hypoxic conditions near the central veins of the liver.

72 ell-localized to hepatocytes surrounding the central veins of the lobules.

73 least 50% narrowing up to total occlusion of central veins of the thorax including superior vena cava

74 s acting like stem cells, located around the central vein or distributed throughout the liver lobule

75 er demonstrated mild liver injury associated central vein outflow obstruction and minimal to moderate

76 We further demonstrate that portal and central vein proximal hepatocytes retain their metabolic

77 tion of a Swan Ganz catheter in a thrombosed central vein, resulted in pulmonary emboli that passed t

78 nd T2* weighted images were used to identify central vein sign (CVS) within the trigeminal lesions.

79 ensitive sequences for the assessment of the central vein sign and paramagnetic rim lesions, which ca

80 ating evidence corroborates the role of the "central vein sign" in the radiological diagnosis of mult

81 The central vein sign, paramagnetic rim lesions, and kappa f

82 cs more specific to multiple sclerosis (e.g. central vein sign, subpial demyelination and lesional ri

83 and immunostaining of metabolic, portal, and central vein-specific markers revealed that hepatocyte p

84 ty and specificity for detection of thoracic central vein stenosis or occlusion.(C) RSNA, 2020See als

85 w devices for the treatment of patients with central vein stenosis.

86 FDG-PET identified central vein STP in five patients, whereas DS and venogr

87 centrilobular hepatocytes surrounding larger central vein structures.

88 fuse C4d deposition along the portal stroma, central vein, subendothelial and stromal space in the pa

89 ion, and directionally from granuloma to the central veins, suggested that substances released from s

90 in delivery) versus delivered to the hepatic central vein (therefore effectively providing a systemic

91 parenchyma, as well as penetration into the central veins, these cells underwent apoptotic cell deat

92 and acute liver cell necrosis, together with central vein thrombosis.

93 ituated in periportal lobular regions to the central vein via a polarized sinusoidal network.

94 ition was eventually not diagnosed as MS had central veins visible in a minority of lesions.

95 condition was eventually diagnosed as MS had central veins visible in the majority of brain lesions a

96 Venopathy of the central vein was also common (63%) and was associated wi

97 The central veins were divided into seven segments for evalu

98 teral veins in 24 patients in whom all major central veins were occluded.

99 -positive bile ducts or veins and 61% +/- 1% central veins were TNF positive; by 48 hours, 57% +/- 1%

100 minary stages of a complete occlusion of the central vein, wich are subsumed under the term venous st

101 st in the portal area, decreasing toward the central vein with the weakest signal in pericentral hepa