ライフサイエンスコーパス: graft thrombosis

1 ntiphospholipid antibodies increases risk of graft thrombosis.

2 Graft failures with UW resulted from graft thrombosis.

3 enced a symptomatic or asymptomatic vascular graft thrombosis.

4 he first 90 days largely related to pancreas graft thrombosis.

5 allograft venous outflow drainage that risk graft thrombosis.

6 y would not result in a reduced frequency of graft thrombosis.

7 aspirin and clopidogrel in the prevention of graft thrombosis.

8 ACE inhibition in reducing the risk of acute graft thrombosis.

9 vascular perturbations underlying synthetic graft thrombosis.

10 rejection (AMR), complement activation, and graft thrombosis.

11 age was the most significant risk factor for graft thrombosis.

12 ssion of splenic vein thrombosis to complete graft thrombosis.

13 ly significant reduction in the incidence of graft thrombosis.

14 te rejection (17.0% vs. 12.1%), and pancreas graft thrombosis (2.6% vs. 1.3%).

15 arotomy were hemorrhage (59.3%) and vascular graft thrombosis (22.2%).

16 ction and graft pancreatitis (38%), pancreas graft thrombosis (27%), and anastomotic leak (15%).

17 ALI events occurred as a result of surgical graft thrombosis (56%), followed by native vessel in sit

18 sulfate is a novel risk factor for dialysis graft thrombosis after endovascular interventions.

19 ic hypotension with prosthetic arteriovenous graft thrombosis after multivariable adjustment.

20 Reexploration for suspected graft thrombosis after pancreas transplantation resulted

21 Vascular graft thrombosis and bleeding are two major issues that

22 gram because of an unacceptable incidence of graft thrombosis and death.

23 ion, is the main independent risk factor for graft thrombosis and early graft loss after renal transp

24 lant IgA-aB2GP1 was the main risk factor for graft thrombosis and early graft loss.

25 type, including PAD resulting from surgical graft thrombosis and in-situ thrombosis.

26 from a combination of primary nonfunction or graft thrombosis and sepsis.

27 targeted gene therapy to prevent acute vein graft thrombosis and the use of folic acid to limit graf

28 ing leaking at the enteric anastomosis site, graft thrombosis, and intraabdominal abscess formation h

29 fect the incidence of polytetrafluorethylene graft thrombosis, and they thus represent a potential tr

30 This study revealed that bile leakage and graft thrombosis are independent and strong risk factors

31 hrombotic therapy in the prevention of renal graft thrombosis are scarce.

32 Graft thrombosis as a cause of graft failure was seen in

33 pathology of the pancreas varied widely with graft thrombosis as the most common finding.

34 the main cause for early graft loss is renal graft thrombosis because kidney transplant outcomes have

35 arried out, obtaining patients with complete graft thrombosis by Doppler ultrasound.

36 Several risk factors to develop graft thrombosis depending on donors and recipients are

37 aft function, early rejection treatment, and graft thrombosis did not differ.

38 The incidence of graft thrombosis fell from 48% in 1988 to 17% in 1994 (P

39 Graft thrombosis following pancreas transplantation is t

40 Patients with graft thrombosis had higher free and total indoxyl sulfa

41 articipants who had not experienced previous graft thrombosis (hazard ratio, 0.52; 95% CI, 0.22 to 1.

42 e interval, 4.81-9.37) and, prominently, for graft thrombosis (hazard ratio, 14.75; 95% confidence in

43 The incidence of graft thrombosis in group 1 (31.2%) was significantly hi

44 primary nonfunction; one living-related for graft thrombosis in the face of fungal infection and bil

45 associated with a lower rate of fistula and graft thrombosis, independent of intradialytic hypotensi

46 No major surgical complications such as graft thrombosis, intra-abdominal infection, or abscess

47 Graft thrombosis is the most common cause of early graft

48 Pancreas graft thrombosis is the most common cause of technical g

49 Hemodialysis access (fistula or graft) thrombosis is an unfortunately common and costly

50 Gene therapy strategies for decreasing graft thrombosis may require expression of antithromboti

51 Graft thrombosis occurred in 0% (0/9) of SK recipients i

52 gA-aB2GP1 was an independent risk factor for graft thrombosis (odds ratio, 5.047; P < 0.001).

53 y, is most frequently caused by acute bypass graft thrombosis or in situ thrombosis of a diseased ves

54 Proportion of participants experiencing graft thrombosis or radiological or surgical interventio

55 n groups regarding bile leakage (P < 0.001), graft thrombosis (P = 0.002), transcystic catheter (P =

56 ary endpoints were the incidence of vascular graft thrombosis, postoperative sepsis, patient, and gra

57 Early postoperative graft thrombosis remain a challenge with pediatric en bl

58 leak (n = 7), aortoduodenal fistula (n = 2), graft thrombosis/stenosis (n = 7), limb separation or fa

59 s a significant decrease in the incidence of graft thrombosis; the authors believe this lower inciden

60 One patient developed stent-graft thrombosis; the prior biliary-TIPS fistula was see

61 We estimated that the odds of graft thrombosis was 1.67 times higher in DCD organs (95

62 Graft thrombosis was found on routine Doppler ultrasound

63 Using multivariate Cox regression analysis, graft thrombosis was independently predicted by absolute

64 Increased incidence of early graft thrombosis was seen in grafts from older donors an

65 was performed monthly for 10 months or until graft thrombosis, with measurement of stenosis at each t

66 Clinical outcomes were partial and complete graft thrombosis within 30 days, bleeding events, relapa

67 subsequent alloantibody formation and led to graft thrombosis without prominent dermal infiltration.