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

6 67 years) who underwent MR venography of the central veins.

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

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

9 all hepatocytes except those encircling the central veins.

10 atic parenchyma and around portal tracts and central veins.

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

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

13 8 hours, 57% +/- 1% portal areas, 40% +/- 1% central veins, and a few sinsusoidal cells expressed TNF

14 recruitment of hepatocytes upstream from the central vein area.

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

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

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

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

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

20 08 who completed the follow-up period of the Central Vein Bypass Study.

21 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 =

22 , 2.15-19.79; p = 0.004), and retention of a central vein catheter (AOR, 6.21; 95% CI, 3.02-12.77; p

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

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

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

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

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

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

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

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

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

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

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

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

35 Adjacent central vein endothelial cells provide Wnt signals that

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

56 centrilobular hepatocytes surrounding larger central vein structures.

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

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

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

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

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

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

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

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

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