ライフサイエンスコーパス: islet transplant

1 ne of the factors crucial for the success of islet transplant.

2 d alpha-CD3-IT, three of whom had a pancreas islet transplant.

3 stered on days -1, 3, and 10 relative to the islet transplant.

4 s and delayed recurrent disease in syngeneic islet transplants.

5 disease in NOD/scid recipients of syngeneic islet transplants.

6 ted CD4 T cells to reject skin, cardiac, and islet transplants.

7 ic mice using either FIV-infected or control islet transplants.

8 rafts achieved results similar to autologous islet transplants.

9 discontinuation of treatment and removal of islet transplants.

10 of disease or allow sustained engraftment of islet transplants.

11 onsible for the failure of a large number of islet transplants.

12 a faster than animals with renal subcapsular islet transplants.

13 Sixteen participants received a total of 26 islet transplants.

14 disease and to contribute to the failure of islet transplants.

15 h chronic failure has appeared for liver and islet transplants.

16 unawareness received intraportal allogeneic islet transplants.

17 to the formation of new blood vessels within islet transplants.

18 es and to improve the survival of pancreatic islets transplants.

19 success depends on the number and quality of islets transplanted.

20 tible angiogenic scaffold received syngeneic islet transplants 2 weeks later.

21 HC II chimera protected syngeneic pancreatic islet transplants against the islet-reactive CD4 T cells

22 I diabetics a year, but at current rates of islet transplant, all recipients could be transplanted w

23 orable decline in insulin independence after islet transplant alone (ITA) has raised concern about it

24 t infusions (SI) in recipients of allogeneic islet transplant alone, displaying GDF.

25 nce at 1 year is lower than what reported in islet transplant alone.

26 wo combined pancreas-kidney transplants, one islet transplant and three double lung transplants were

27 approximately 150 mg/dl) in 10 recipients of islet transplants and 10 control subjects.

28 cells are also recruited to CCL22-expressing islet transplants and are required for CCL22-mediated pr

29 ed independence after one (3/5) or two (2/5) islet transplants and remained independent while on EFA

30 eceived NOD severe combined immunodeficiency islet transplants and were treated with daily LSF inject

31 a linear relationship between the number of islets transplanted and luminescence intensity.

32 able kidney allografts 1-11 years before the islet transplant, and one patient had a simultaneous isl

33 results, while occasional early failures of islet transplants are still observed.

34 Even when single donor islet transplants become the norm, there will still be m

35 ers of native islets available in autologous islet transplant candidates and is a means of following

36 Furthermore, in contrast to the islet transplants, CCR2 deficiency offered only marginal

37 onses correlated robustly with the number of islets transplanted (correlation coefficients range 0.81

38 of an immunosuppressive agent at the site of islet transplant could promote long-term engraftment wit

39 t comprehensive collection of human-to-human islet transplant data.

40 not observed in recipients with functioning islet transplants, despite the continuous need for exoge

41 In untreated controls, marginal mass islet transplants did not restore euglycemia.

42 allogeneic barriers, whereas nonvascularized islet transplants did not.

43 an intramuscular site significantly improves islet transplant engraftment and survival compared with

44 In the xenogeneic model, we quantified islet transplant exosomes in recipient blood over long-t

45 toimmunity is an important factor leading to islet transplant failure in autoimmune diabetic BB rats.

46 ty has usually been discounted as a cause of islet transplant failure.

47 ng beta-cells, and it may also contribute to islet transplant failure.

48 extend this approach to cellular transplant, islet transplant from the same donor was attempted in th

49 ion of 23 years (range 18-29 years) received islet transplants from 1 to 5 donors.

50 in-induced diabetic CBA (H-2k) mice received islet transplants from BALB/c (H-2d) donors.

51 e: 1) Encapsulation technology that protects islet transplants from host immune surveillance; 2) stem

52 Islets transplanted from other species to man has the po

53 roved when compared with short-term cultured islets transplanted from the same preparation (P<0.01).

54 a uniquely demonstrate that: 1) intrahepatic islet transplant grafts secrete glucagon in response to

55 mia during and after exercise, the rats with islet transplants had significantly lower blood glucose

56 ion of HSCs impaired tolerance to allogeneic islet transplants in B6 recipients.

57 ence leading to the destruction of syngeneic islet transplants in diabetic NOD mice.

58 te exercise caused hypoglycemia in rats with islet transplants in different sites including liver, ki

59 r pancreatic lymph node cells (PLNC) protect islet transplants in Non-obese diabetic (NOD) mice.

60 In this study, using an in vivo model of islet transplants in TCR transgenic mice, we show that b

61 ndiabetogenic regimen in a clinical trial of islet transplants in type 1 diabetic recipients.

62 lin and C-peptide responses to the number of islets transplanted in each recipient for comparison wit

63 5-HTP signal was compared with the number of islets transplanted in rats.

64 versus naked (MRT, 36 days; P < 0.01) baboon islets transplanted in the EFP site.

65 Islets transplanted in the liver appeared as distinct si

66 Glucagon responses to hypoglycemia from islets transplanted in the liver are defective.

67 protocol (i.e., one or if necessary a second islet transplant), insulin independence has been achieve

68 Syngeneic islets transplanted into a SC, neovascularized device re

69 t endothelial cells was also seen with human islets transplanted into an immunodeficient mouse model.

70 Human islets transplanted into diabetic immunodeficient mice r

71 Control islets transplanted into diabetic mice were rejected in

72 e tolerance, and pancreatic apoCIII knockout islets transplanted into diabetic mice, with high system

73 BALB/c islets transplanted into hyperglycemic NOD mice under pr

74 Pancreatic islets transplanted into immunocompetent diabetic subjec

75 Syngeneic islets transplanted into mice cured by treatment with AL

76 s but were in the range of 0.2-0.5% in human islets transplanted into mice.

77 thway promote beta-cell replication in human islets transplanted into NOD-scid IL-2Rg(null) mice.

78 vasive, longitudinal detection of pancreatic islets transplanted into non-human primates using a low-

79 on to glucose was compared to the ability of islets transplanted into nondiabetic NOD-SCID mice to se

80 Although porcine islets transplanted into nonimmunosuppressed macaques we

81 erglycemia on primary function of allogeneic islets transplanted into spontaneously diabetic recipien

82 longitudinal in vivo confocal microscopy of islets transplanted into the anterior chamber of the eye

83 Mouse islets transplanted into the CP routinely restored glyce

84 s were found after exercise in the rats with islets transplanted into the liver (62 +/- 6, 165 +/- 29

85 strate the occurrence of amyloid deposits in islets transplanted into the liver in three of four pati

86 lantation, and correlated with the number of islets transplanted into the liver or kidney.

87 rease was found in controls and in rats with islets transplanted into the peritoneal cavity or under

88 Macroencapsulated islets transplanted into the s.c. space were able to sur

89 Rat islets transplanted into the spleen were visualized in v

90 n was also observed by using IL-18-deficient islets transplanted into WT recipients, demonstrating th

91 comparing the transplant outcomes to that of islets transplanted intraportal.

92 vasive assessment of the liver receiving the islet transplant is important to evaluate the status isl

93 an predict islet graft survival in type 1 DM islet transplant (ITx) recipients.

94 lly reduced inflammatory cell migration into islet-transplanted liver in MMP-9 knockout recipients.

95 I) modalities are being developed to monitor islet transplant mass and function in vivo.

96 lantation heparin and insulin infusions, and islet transplant mass remained significant.

97 seline, donor weight, donor body mass index, islet transplant mass, and peritransplant heparin and in

98 distribution of islet grafts in the liver of islet-transplanted mice.

99 hypothesis in a human-into-mouse xenogeneic islet transplant model and validated the concept in clin

100 o, both a syngeneic (B6-to-B6) marginal mass islet transplant model to assess the impact of TLR4 bloc

101 s in vivo, a renal subcapsular marginal mass islet transplant model was developed in streptozotocin-i

102 Finally, in the MHC-matched islet transplant model, Lef could not significantly prol

103 Using a nonhuman primate islet transplant model, RATG plus sirolimus supports isl

104 Using an immunocompromised marginal mass islet transplant model, the ability of Ad-IGF-II-transdu

105 In a rat-to-mouse xenogeneic islet transplant model, we show that rat ECDI-SPs alone

106 We recently developed a dual islet transplant model, which enables direct histologic

107 ate the alloimmune response was tested in an islet transplant model.

108 anced islet engraftment in this large animal islet transplant model.

109 nd human in vitro systems and in vivo murine islet transplant models, using species-specific anti-TLR

110 Neonatal porcine islet transplanted NOD-SCID IL2rgamma(-/-) mice received

111 ll), and splenocytes were cotransferred into islet transplanted nonobese diabetic background with sev

112 ently, we compared the ability of suboptimal islet transplants of 50 or 125 syngeneic islets to achie

113 By bioluminescence imaging, islets transplanted on a polymer scaffold remain localiz

114 Islets transplanted on scaffolds retained the architectu

115 Islet transplant outcome was analyzed in 59 consecutive

116 mechanisms that are involved in determining islet transplant outcome.

117 dies demonstrate that mHGF markedly improves islet transplant outcomes in the highest preclinical spe

118 poptosis in vitro and significantly improved islet transplant outcomes in vivo.

119 leased, and high levels correlated with poor islet transplant outcomes.

120 tribution in a preparation may contribute to islet transplant outcomes.

121 idonor sensitization and adversely impacting islet transplant outcomes.

122 od mononuclear cells obtained from long-term islet-transplanted patients showed an increased percenta

123 , who died two years after the second of two islet transplants performed using the Edmonton protocol.

124 al human pancreas samples, obtained from the islet transplant program at the University of Minnesota,

125 center, we have established a collaborative islet transplant program between two geographically dist

126 the equitably available, fully integrated UK islet transplant program with both transported and local

127 ars of the UK's nationally funded integrated islet transplant program.

128 n procurement organizations and pancreas and islet transplant programs.

129 mus levels monitorization, should be part of islet transplant recipient care.

130 Furthermore, serum from an islet transplant recipient who developed anti-class II a

131 A validation cohort of islet transplant recipients (n = 114 MMTTs) examined 12

132 satile insulin secretion is reestablished in islet transplant recipients and that glucose-mediated st

133 Recent reports have shown that islet transplant recipients develop antibodies against d

134 A large proportion of clinical islet transplant recipients fail to initially achieve or

135 morphisms between 21 prospectively recruited islet transplant recipients from a single institution an

136 The immune monitoring of islet transplant recipients includes the assessment of p

137 Only a minority of islet transplant recipients maintain insulin independenc

138 ggest that short-term AAT treatment of human islet transplant recipients may be worthy of a clinical

139 ndence (II) have been invariably observed in islet transplant recipients under the "Edmonton protocol

140 Forty islet transplant recipients who completed 344 Health Sta

141 al and laboratory outcomes of 347 allogeneic islet transplant recipients, using data from the Collabo

142 al value under adequate immunosuppression in islet transplant recipients.

143 t and progression of rejection in pancreatic islet transplant recipients.

144 transplant recipients and is universal among islet transplant recipients.

145 actors associated with kidney dysfunction in islet transplant recipients.

146 ntial components of the metabolic testing of islet transplant recipients.

147 rformed this procedure successfully in three islet-transplant recipients each receiving two infusions

148 9); recipients reported to the Collaborative Islet Transplant Registry (CITR) given TCDAb+TNF-alpha-i

149 d to the NIDDK and JDRF funded Collaborative Islet Transplant Registry (CITR), currently the most com

150 ecipients, using data from the Collaborative Islet Transplant Registry (CITR).

151 of alloislet recipients in the Collaborative Islet Transplant Registry.

152 ponses were highly correlated to the mass of islets transplanted (response to glucose: r = 0.84, P <

153 al expression of FasL on cellular as well as islet transplants results in accelerated rejection by ne

154 he progressive loss of beta-cell function in islet transplants seems unlikely to be explained by allo

155 After each islet transplant, she gradually lost insulin independenc

156 Ex vivo analysis of the islet transplant showed colocalization of tracer accumul

157 s that the epididymal fat pad maybe a useful islet transplant site in the mouse model for effective g

158 islet allografts implanted at two different islet transplant sites (liver and kidney capsule [KC]) w

159 In contrast, islets transplanted subcutaneously alone failed to engra

160 ss these issues, we compared the survival of islet transplants (subject to tissue-specific autoimmuni

161 ery of HGF to murine islets ex vivo improves islet transplant survival and blood glucose control in a

162 t and immune suppression that have increased islet transplant survival, graft function progressively

163 till be more patients who might benefit from islet transplants than grafts available.

164 To increase the number of islet transplants, the suitability of pancreases from or

165 Two of the latter animals received a second islet transplant, this time to the portal system, and bo

166 All (14/14) WF and 75% (6/8) BN islet transplants to BB-Ac recipients failed after a mea

167 One cohort of Brown Norway (BN) islet transplants to BB-Ac with CsA was performed.

168 For islet transplants to complete the transition from clinic

169 Revascularization of islets transplanted to MMP-9-deficient mice was impaired

170 led function-equivalent BDD islets, and NHBD islets transplanted to non-obese diabetic-severe combine

171 In contrast, porcine islets transplanted to the liver subcapsular space do no

172 Pancreatic islets transplanted to treat autoimmune type 1 diabetes

173 These results indicate that autologous islets, transplanted to the canine thymus, engraft, func

174 g the designs and analyses of future phase 3 islet transplant trials, we analyzed key clinical and la

175 uced a marked prolongation of survival of WF islets transplanted under the kidney capsule of diabetic

176 Mouse islets transplanted under the renal capsule of cynomolgu

177 t cell mass transplantation model (200 mouse islets transplanted under the renal capsule of syngeneic

178 Normal mice and mice with islets transplanted under the renal capsule or under the

179 mmunosuppressive and can effectively protect islet transplants via induction of MDSCs.

180 ne whether the late failure of beta-cells in islets transplanted via the portal vein is caused by exc

181 raft function over 12 months following first islet transplant was determined prospectively in consecu

182 In contrast, survival of fresh islet transplants was not significantly improved by this

183 BLI of mice bearing islet transplants was seen in the expected anatomic loca

184 To determine insulin secretory reserve after islet transplant, we performed studies of glucose potent

185 De novo DSA directed against most recent islet transplant were absolutely associated with loss of

186 Islet transplants were performed under kidney capsule of

187 orically, these have included pancreatic and islet transplants, which were later combined with treatm

188 Eventually, islet transplants will replace pancreas transplants for

189 eatic islet reserve, they underwent a second islet transplant with 326,720 and 768,132 IEQ, respectiv

190 severely diabetic mice required minimal dose islet transplant with nIgM to restore normoglycemia (n =

191 nflammatory mediators in patients undergoing islet transplants within hours of infusion.

192 dence has established definitive survival of islets transplanted within the thymus of a phylogenetica

193 evelopment of T1D or to promote tolerance to islet transplants without using immunosuppressive drugs

194 ahepatically transplanted islets compared to islets transplanted without a scaffold.

195 where blood perfusion was less decreased in islets transplanted without prior culture and in many ca