ライフサイエンスコーパス: nonfunction

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

2 ary cause of graft failure was primary graft nonfunction.

3 with a high risk of dysfunction and primary nonfunction.

4 genes may prevent beta cell loss and primary nonfunction.

5 She subsequently died secondary to primary nonfunction.

6 ion variables and less graft loss to primary nonfunction.

7 ematurity was a risk factor for thrombus and nonfunction.

8 h to protect marginal grafts against primary nonfunction.

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

10 tion for graft failure not caused by primary nonfunction.

11 diators that can contribute to islet primary nonfunction.

12 ft loss from vascular thrombosis and primary nonfunction.

13 ells play an important role in primary graft nonfunction.

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

15 ar necrosis, vascular thrombosis, or primary nonfunction.

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

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

18 y graft function; two recipients had primary nonfunction.

19 ence of poor early graft function or primary nonfunction.

20 were used as second grafts for primary graft nonfunction.

21 ecessary to address the high rate of primary nonfunction.

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

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

24 nimizing the recipient risk of primary graft nonfunction.

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

26 One patient had primary nonfunction.

27 the risk of intraoperative death and primary nonfunction.

28 ntation because of increased risk of primary nonfunction.

29 h can ultimately lead to apoptosis and graft nonfunction.

30 lure following retransplantation for primary nonfunction.

31 cm in diameter that appear to be clinically nonfunctioning.

32 There were no cases of primary nonfunction, 1 case of postreperfusion syndrome (9%) and

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

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

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

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

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

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

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

40 e) failed to predict graft survival, primary nonfunction, 90-d graft loss, or mortality.

41 rvival, with delayed graft function, primary nonfunction, acute rejection, estimated glomerular filtr

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

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

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

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

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

47 Thirty percent of pituitary adenomas are nonfunctioning adenomas, which do not produce hormones.

48 uppression test (serum cortisol: <50 nmol/L, nonfunctioning adrenal tumor [NFAT]; 50 to 138 nmol/L, p

49 Adrenal incidentalomas are mostly benign nonfunctioning adrenal tumors (NFATs) or adenomas causin

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

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

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

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

54 adjusted HR [aHR], 0.39 [95% CI, 0.27-0.57]; nonfunctioning: aHR, 0.29 [95% CI, 0.16-0.56]), grade of

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

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

57 so demonstrated a lower incidence of primary nonfunction and biliary strictures, although this differ

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

59 Although the incidence of primary nonfunction and delayed graft function is higher with or

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

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

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

63 non-anastomotic biliary strictures, primary nonfunction and hepatic artery thrombosis were observed

64 rafts are known to be predisposed to primary nonfunction and ischemic cholangiopathy.

65 or transplantation, while preventing primary nonfunction and minimizing ischemic cholangiopathy.

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

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

68 Primary nonfunction and primary dysfunction formed the main caus

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

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

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

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

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

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

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

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

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

78 y leading to delayed graft function, primary nonfunction, and sometimes rejection.

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

80 logeneic islet transplantation had a primary nonfunction, as shown by measurable posttransplantation

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

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

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

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

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

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

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

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

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

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

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

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

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

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

95 ft-associated complications, such as primary nonfunction, delayed graft function, or late biliary inj

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

97 ymoglobulin group who suffered primary graft nonfunction died.

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

99 injury resulting in a higher rate of primary nonfunction, early allograft dysfunction and posttranspl

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

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

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

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

104 ferences for delayed graft function, primary nonfunction, estimated glomerular filtration rate, and a

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

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

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

108 Primary nonfunction, graft failure, and recipient death correlat

109 focusing on delayed graft function, primary nonfunction, graft function, graft survival, and graft u

110 Outcomes assessed included rates of primary nonfunction, graft survival, and patient survival.

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

112 information inferred is adequate to exclude nonfunctioning grafts but is limited in evaluating compr

113 no guidelines for the management of clotted nonfunctioning grafts.

114 One graft with primary nonfunction had low rate of factor accumulation.

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

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

117 ates of early allograft dysfunction, primary nonfunction, hepatic artery thrombosis, biliary ischemia

118 rtem heparin reported lower rates of primary nonfunction, hepatic artery thrombosis, graft failure at

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

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

121 F was observed in 36% (n = 1321) and primary nonfunction in 3% (n = 122) of recipients.

122 d normocomplementemic rats underwent primary nonfunction in all animals.

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

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

125 Whether low concentrations predict nonfunction in high-risk livers with severe injury requi

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

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

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

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

130 The median incidence of primary nonfunction in uDCD was 12.3% versus 5.7% for cDCD (RR,

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

132 contamination can ultimately lead to primary nonfunction in vivo.

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

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

135 during kidney function intervals than during nonfunction intervals.

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

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

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

139 ents developed an atrophic retinal hole in a nonfunctioning macular area where baseline OCT showed pr

140 or in the most extreme cases, primary graft nonfunction necessitating urgent regrafting.

141 rnative second-line therapy, particularly in nonfunctioning NETs and patients with SSTR-negative tumo

142 ded similar outcomes with respect to primary nonfunction (NMP 3.3% and NRP 5.6%), graft function (12-

143 Two patients, one with benign nonfunctioning nodules and one with functioning thyroid

144 All patients with primary nonfunctioning, nonmetastatic well/moderately differenti

145 Primary nonfunction occurred in 2.2% of all SCS (n=3, p =0.10).

146 Primary nonfunction occurred in 60 (1.35%) patients in the HTK g

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

148 6; 95% CI, 1.037-1.853), but not for primary nonfunction (odds ratio, 1.342; 95% CI, 0.900-2.002).

149 UW demonstrated respective rates of primary nonfunction of 1.63% vs 0.82% (P = .20), 90-day graft su

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

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

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

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

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

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

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

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

158 table for LT, there were no cases of primary nonfunction or death in the recipients.

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

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

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

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

163 on between mild arteriosclerosis and primary nonfunction (OR, 2.14; 95% CI, 1.19-3.84; P = 0.01).

164 ere more frequently complicated with primary nonfunction (P = 0.013) and early allograft dysfunction

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

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

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

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

169 Ga-DOTATOC PET/CT were falsely positive in 1 nonfunctioning pancreatic neuroendocrine tumor.

170 Nonfunctioning pancreatic neuroendocrine tumors (NF-PanN

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

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

173 IT for the following outcomes: primary graft nonfunction (PGNF), delayed graft function (DGF), estima

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

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

176 In contrast, 70% developed primary nonfunction (PNF) and died in the DCD120'-group.

177 Transplant outcomes, including primary nonfunction (PNF) and early allograft dysfunction, were

178 ression to identify risk factors for primary nonfunction (PNF) and short- and long-term graft surviva

179 Primary nonfunction (PNF) has declined in incidence over the yea

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

181 There are sparse data on the rate of primary nonfunction (PNF) losses and their consequences within K

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

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

184 nd early redo-LT including those for primary nonfunction (PNF) or hepatic artery thrombosis were excl

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

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

187 gression identified risk factors for primary nonfunction (PNF), delayed graft function (DGF), and gra

188 ical test to predict early outcomes [primary nonfunction (PNF), early graft dysfunction (EAD)].

189 plasmapheresis in primary hepatic allograft nonfunction (PNF).

190 iac arrest (7.7% vs 0.3%; P < .001), primary nonfunction (PNF; 7.7% vs 1.0%; P = .003), early allogra

191 Risk factors for primary nonfunction (PNF; n = 37) and poor renal function (estim

192 th (DCD) donors suffer a higher incidence of nonfunction, poor function, and ischemic cholangiopathy.

193 re associated with increased risk of primary nonfunction, poor function, and nonanastomotic stricture

194 discard and somewhat associated with primary nonfunction posttransplant.

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

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

197 ailures, where structural issues and primary nonfunction prevailed, compared to later failures with a

198 s a haploinsufficiency of that protein, or a nonfunctioning protein that subverts the molecular syste

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

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

201 PE was used in 84% of cases, and the primary nonfunction rate was 5%.

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

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

204 othermic regional perfusion improved primary nonfunction rates in uDCD grafts.

205 actors function well with acceptable primary nonfunction rates.

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

207 1.08, 95% CI = 0.63-1.86, P = 0.77), primary nonfunction (relative risk = 0.73, 95% CI = 0.22-2.40, P

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

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

210 Primary nonfunction resulting in immediate graft loss is respons

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

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

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

214 mes included delayed graft function, primary nonfunction, serum creatinine, and biliary complications

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

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

217 ned, there were worsening trends for primary nonfunction, stage 4 chronic kidney disease at 1 year, a

218 The nonfunctioning subunit may provide structural support en

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

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

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

222 fication of mutations of DAXX/ATRX in small, nonfunctioning tumors can predict the malignant progress

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

224 Regardless of size, G1 nonfunctioning tumors with no nodal involvement and vasc

225 Among the 587 resected Pan-NENs, 75% were nonfunctioning tumors, and 5% were syndrome-associated t

226 75 months, recurrence analysis revealed that nonfunctioning tumors, tumor grade, N1 status, and vascu

227 by the secretion of pituitary hormones, and nonfunctioning tumors.

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

229 y graft loss rate from thrombosis or primary nonfunction was 11% for both groups.

230 The rate of primary nonfunction was also significantly higher (P = 0.031) in

231 s were shorter, and the incidence of primary nonfunction was comparable.

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

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

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

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

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

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

238 dysfunction (delayed graft function/primary nonfunction) were significantly lower for female donor k

239 variable of early graft failure and primary nonfunction within 60 d of ITx.

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