ライフサイエンスコーパス: nonfunction

1 x, or cause of graft failure (% with primary nonfunction).

2 She subsequently died secondary to primary nonfunction.

3 ion variables and less graft loss to primary nonfunction.

4 ematurity was a risk factor for thrombus and nonfunction.

5 h to protect marginal grafts against primary nonfunction.

6 curred with 16 kidneys; there was no primary nonfunction.

7 tion for graft failure not caused by primary nonfunction.

8 diators that can contribute to islet primary nonfunction.

9 ft loss from vascular thrombosis and primary nonfunction.

10 ells play an important role in primary graft nonfunction.

11 her than the mouse, a process called primary nonfunction.

12 ar necrosis, vascular thrombosis, or primary nonfunction.

13 on is the major cause of primary islet graft nonfunction.

14 on without the fear of high rates of primary nonfunction.

15 y graft function; two recipients had primary nonfunction.

16 GF) and, in severe cases, results in primary nonfunction.

17 ence of poor early graft function or primary nonfunction.

18 were used as second grafts for primary graft nonfunction.

19 nimizing the recipient risk of primary graft nonfunction.

20 ecessary to address the high rate of primary nonfunction.

21 rvival only 73%, and 12.5% suffering primary nonfunction.

22 nction, and 1 patient (9%) had primary graft nonfunction.

23 One patient had primary nonfunction.

24 the risk of intraoperative death and primary nonfunction.

25 ntation because of increased risk of primary nonfunction.

26 h can ultimately lead to apoptosis and graft nonfunction.

27 lure following retransplantation for primary nonfunction.

28 ary cause of graft failure was primary graft nonfunction.

29 with a high risk of dysfunction and primary nonfunction.

30 genes may prevent beta cell loss and primary nonfunction.

31 cm in diameter that appear to be clinically nonfunctioning.

32 anisms (1.5%), thrombus (0.6%), and catheter nonfunction (10.9%).

33 HBD graft had a greater incidence of primary nonfunction (11.8 vs. 6.4%, P = 0.008) and retransplanta

34 Postoperative complications included primary nonfunction (15%), rejection (85%), graft vascular throm

35 te or chronic rejection (26.6%), and primary nonfunction (16.7%).

36 vascular complications (35%), primary graft nonfunction (22%), rejection (19%), and HCV recurrence (

37 ute rejection, 16% vs. 11% (P=0.11); primary nonfunction, 3% vs. 2% (P=0.38); and wound complications

38 luded vascular complications (43%) and graft nonfunction (40%), whereas leading causes of death were

39 e 3 (MEG3) is selectively lost in clinically nonfunctioning adenomas (NFAs) of gonadotroph origin; ho

40 Clinically nonfunctioning adenomas account for 15% to 54% of adenom

41 mptoms of hormone excess, whereas those with nonfunctioning adenomas often present later and have sym

42 Only one of five clinically nonfunctioning adenomas, a gonadotroph luteinizing hormo

43 ious histologic types include prolactinomas, nonfunctioning adenomas, somatotropinomas, corticotropin

44 nction and an increased incidence of primary nonfunction after liver transplantation.

45 nt transplant-related complications: primary nonfunction after retransplantation (liver), cytomegalov

46 Fatty livers are more prone to primary nonfunction after transplantation.

47 R<30 ml/min per 1.73 m(2) (including primary nonfunction) after 1 year.

48 Primary graft nonfunction and 30-day mortality rates were higher and 1

49 ever, there was a lower incidence of primary nonfunction and a longer posttransplant survival time in

50 ociated with an unacceptable risk of primary nonfunction and delayed graft failure.

51 th posttransplant graft dysfunction (primary nonfunction and delayed graft function) and were an inde

52 The etiology of primary graft nonfunction and dysfunction is unknown but most likely i

53 no significant difference regarding primary nonfunction and dysfunction, hepatic artery and biliary

54 ent retransplantation, one for primary graft nonfunction and one because of biliary cast syndrome wit

55 The incidence of primary nonfunction and poor early graft function was 5% and 10%

56 Primary nonfunction and primary dysfunction formed the main caus

57 her incidence of graft loss owing to primary nonfunction and technical complications (9 vs. 2, P<0.05

58 ies of OA can prevent nonimmunologic primary nonfunctioning and immunologic phenomena ascribed to gra

59 function, 2 patients (6%) had primary graft nonfunction, and 1 patient (3%) had early graft loss.

60 minotransferase and total bilirubin, primary nonfunction, and 30-day and 1-year graft survival.

61 thrombosis, portal vein thrombosis, primary nonfunction, and biliary stricture between the two group

62 Primary graft nonfunction, and immediate, 1-year, and 2-year mortality

63 th with function, technical failure, primary nonfunction, and recurrent disease) in Group 2 was 91%.

64 th with function, technical failure, primary nonfunction, and recurrent disease, leaving 1587 recipie

65 ft failure were vascular thrombosis, primary nonfunction, and sepsis.

66 usion syndrome, poor graft function, primary nonfunction, arterial thrombosis, biliary complication,

67 ability to predict graft failure or primary nonfunction at liver transplant decision time assists ut

68 regulate prespore expression when fused to a nonfunctioning basal promoter.

69 Two instances of primary renal allograft nonfunction because of cholesterol embolization are repo

70 The differences in primary nonfunction between kidneys from uDCD and cDCD were expl

71 edure for lowering IOP in eyes with ischemic nonfunctioning blebs and patent trabeculectomy ostia.

72 All eyes had ischemic nonfunctioning blebs with patent internal ostia and unde

73 monoclonal antibody (mAb) GoH3, but not by a nonfunction blocking anti-alpha6 mAb, or by mAbs against

74 a(6) monoclonal antibody, GoH3, but not by a nonfunction-blocking anti-alpha(6) monoclonal antibody.

75 mited by the need to microinject dye-labeled nonfunction-blocking antibodies.

76 he possible role of free radicals in primary nonfunction caused by acute ethanol.

77 ular competition) can delay aging by purging nonfunctioning cells.

78 s for multiple retransplant included primary nonfunction, chronic rejection, hepatic artery thrombosi

79 potentially reduce the incidence of primary nonfunction, decrease the immunogenicity of the cold inj

80 ough they have higher rates of primary graft nonfunction, delayed graft function, discard, and retrie

81 p of AKI with delayed graft function/primary nonfunction (DGF/PNF), estimated glomerular filtration r

82 ymoglobulin group who suffered primary graft nonfunction died.

83 a significant risk factor for primary graft nonfunction due to increased sensitivity to ischemia rep

84 iated with an increased incidence of primary nonfunction, early allograft dysfunction, and biliary st

85 based on the removal of volume-occupying but nonfunctioning emphysematous lung, which is thought to i

86 primary tumors, including 12 insulinomas, 28 nonfunctioning endocrine tumors, and four acinar carcino

87 ations, we now recommend elective removal of nonfunctioning, enterically drained pancreas allografts.

88 If censored for primary nonfunction, estimated glomerular filtration rates after

89 mas, 5 were Hurthle cell carcinomas, 21 were nonfunctioning follicular adenomas, and 9 were Hurthle c

90 ant/subfulminant hepatic failure and primary nonfunction following liver transplantation were include

91 Primary nonfunction, graft failure, and recipient death correlat

92 These findings suggest that clotted nonfunctioning grafts are frequent harbingers of infecti

93 no guidelines for the management of clotted nonfunctioning grafts.

94 cal relevance of silent infection in clotted nonfunctioning hemodialysis grafts, a study was conducte

95 underwent retransplants; mainly for primary nonfunction, hepatic artery thrombosis, and recurrent pr

96 ally resected human invasive PAs and in the (nonfunctioning) HP75 human pituitary tumor-derived cell

97 tion for graft failure not caused by primary nonfunction identified preoperative serum bilirubin and

98 d normocomplementemic rats underwent primary nonfunction in all animals.

99 The incidence of primary nonfunction in animals receiving a four-drug immunosuppr

100 vasoplegia; 1 recipient experienced primary nonfunction in conjunction with a difficult explant.

101 There may be an increased risk of primary nonfunction in livers procured from donors with hypernat

102 in three to four (0.6% to 0.8%) and primary nonfunction in one (0.2%).

103 There was a higher incidence of primary nonfunction in the DKT group, although the incidence of

104 There was a significantly higher rate of nonfunction in the subjective group (17.1%), compared to

105 Primary nonfunction in uDCD was higher than in the cDCD (19.6% v

106 contamination can ultimately lead to primary nonfunction in vivo.

107 s (time with a transplant) with incidence in nonfunction intervals (waitlist or time after transplant

108 nd kidney and thyroid cancers (higher during nonfunction intervals).

109 during kidney function intervals than during nonfunction intervals.

110 ntify differentially expressed genes between nonfunctioning invasive and noninvasive PAs.

111 e 1 diabetes often fail to function (primary nonfunction), likely because of islet beta-cell apoptosi

112 Despite similar rates of primary nonfunction, LTx after controlled DCD resulted in worse

113 ailure due to intrahepatic cholangiopathy or nonfunction occurred in HOPE-treated livers, whereas 18%

114 6; 95% CI, 1.037-1.853), but not for primary nonfunction (odds ratio, 1.342; 95% CI, 0.900-2.002).

115 s not appear to play a major role in primary nonfunction of canine islet xenografts in nonimmunosuppr

116 y has been used for the treatment of primary nonfunction of hepatic allografts and fulminant hepatic

117 zyme A reductase inhibitor, prevents primary nonfunction of islet isografts by reducing inflammatory

118 Prompt retransplantation for primary graft nonfunction of older donors are generally more cholestat

119 ife support reduced the incidence of primary nonfunction of the allograft.

120 recurrent infection, and 3 (7%) died (2 from nonfunction of the primary graft and 1 from complication

121 rane attack complex of complement in primary nonfunction of transplanted xenoislets.

122 our retransplants (two cadaveric for primary nonfunction; one living-related for graft thrombosis in

123 od (< 1 month) from a combination of primary nonfunction or graft thrombosis and sepsis.

124 There was no primary graft nonfunction or intraoperative right heart failure.

125 llografts, 8 were omitted because of primary nonfunction or postoperative complications.

126 y allograft failure because of primary graft nonfunction or vascular complications, six patients with

127 ect is more marked in transformed cells with nonfunctioning p21WAF1 or p53 genes.

128 ed 29 Dutch patients with a pathology-proven nonfunctioning pancreatic NET treated with (177)Lu-octre

129 , the median PFS in 90 other patients with a nonfunctioning pancreatic NET with more than 3 liver met

130 In the present study, 12 gastrinoma and nonfunctioning pancreatic neuroendocrine tumor specimens

131 Nonfunctioning pancreatic neuroendocrine tumors (NF-PanN

132 After exclusion of primary nonfunction patients, survival was 73% for BAL versus 59

133 ransplanted for acute reasons (primary graft nonfunction (PGNF) or hepatic artery thrombosis [HAT]),

134 It is now recognized that most clinically nonfunctioning pituitary tumors express gonadotropin hor

135 kidneys but is associated with more primary nonfunction (PNF) and delayed graft function (DGF).

136 Primary nonfunction (PNF) is a devastating outcome after kidney

137 n group 2 (n = 3) were patients with primary nonfunction (PNF) of a transplanted liver, and in group

138 Current diagnostic criteria for primary nonfunction (PNF) of liver grafts are based on clinical

139 d points were incidence of primary allograft nonfunction (PNF) or severe renal dysfunction.

140 The overall incidence of primary graft nonfunction (PNF) was 7.6%.

141 plasmapheresis in primary hepatic allograft nonfunction (PNF).

142 uired excision of the pouch, 32 (0.8%) had a nonfunctioning pouch, and 46 patients (1.2%) had redo IP

143 for a given recipient can result in primary nonfunction, premature graft failure, or inappropriate d

144 There was a significantly greater primary nonfunction rate in sensitized patients in spite of simi

145 For DCD, the primary nonfunction rate was 5% and delayed graft function was 2

146 essment by the procuring surgeon have a high nonfunction rate, associated with a high morbidity.

147 Recently reported primary nonfunction rates are similar to those of LT using graft

148 actors function well with acceptable primary nonfunction rates.

149 and RB1 and that in tumor cell lines with a nonfunctioning RB1, reduction of gamma-tubulin protein l

150 1.08, 95% CI = 0.63-1.86, P = 0.77), primary nonfunction (relative risk = 0.73, 95% CI = 0.22-2.40, P

151 re present in 57% of the patients with early nonfunction renal allografts and 35% of the patients wit

152 rossmatch sera from 56 patients with primary nonfunctioning renal allografts were tested for aPA.

153 Primary nonfunction resulting in immediate graft loss is respons

154 were the risk of early dysfunction, primary nonfunction, retransplantation, patient survival, and gr

155 ks of free access to either a functioning or nonfunctioning running wheel.

156 Following stress exposure, functioning or nonfunctioning running wheels were introduced into stres

157 On the previously nonfunctioning side, there were substantial changes in V

158 differentiated or moderately differentiated, nonfunctioning, somatostatin receptor-positive neuroendo

159 The nonfunctioning subunit may provide structural support en

160 dimer pair there is one functioning and one nonfunctioning subunit.

161 ight participate in the induction of primary nonfunction through a number of mechanisms.

162 er rates of graft dysfunction due to primary nonfunction traditionally observed in NHBD.

163 re of choice for most benign functioning and nonfunctioning tumors of the adrenal gland.

164 rgery for ACTH-secreting, TSH-secreting, and nonfunctioning tumors; it is less commonly required for

165 II NHB donor where the incidence of primary nonfunction was high, illustrated by phase II where mach

166 Delayed nonfunction was identified in one recipient of a left lo

167 The retransplantation rate for primary graft nonfunction was not significantly different from group A

168 However, primary nonfunction was observed in all animals when islet trans

169 table to the product and no cases of primary nonfunction were observed.

170 c-type biliary stricture (ITBS), and primary nonfunction were similar between groups.

171 Patients listed for primary nonfunction within 7 days of OLT (n = 268) did not show