ライフサイエンスコーパス: isograft

1 recipients (allografts) or the same strain (isografts).

2 enal subcapsular transplantation of an islet isograft.

3 10 (50%) of 20 PRKO mice without a pituitary isograft.

4 otec on the individual tissues of a rat limb isograft.

5 polymorphonuclear leukocyte influx into the isograft.

6 in the cellular infiltrates around the islet isografts.

7 were significantly decreased in transplanted isografts.

8 ng growth factor-beta in these cold-ischemic isografts.

9 re tested for their ability to reject second isografts.

10 ifferences between control and cold ischemic isografts.

11 M-1 and cytokines comparable to that seen in isografts.

12 own in both transfected COS7 cells and heart isografts.

13 infiltration was greater in allografts than isografts.

14 Group 4 rats (n=3) received isografts.

15 cies; (4) DMBA alone; and (5) DMBA+pituitary isografts.

16 n in isografts, but IL-4 was detected in 3/5 isografts.

17 mpared with acutely rejecting allografts and isografts.

18 t bm12 allografts appeared no different than isografts.

19 titate the intensity of antibody staining in isografts.

20 ee in the immediately adjacent myocardium in isografts.

21 ion after 18-h culture than cells from liver isografts.

22 challenge, allografts, or without challenge, isografts.

23 l as in intimal thickness when compared with isografts.

24 EIIIB+ FN ratios remain relatively low in isografts.

25 nhance nerve regeneration in the same way as isografts.

26 irway lumen, changes not seen in heterotopic isografts.

27 DBA/2 kidneys or B6.Foxp3(DTR) recipients of isografts.

28 ected into the rNG and the resident cells of isografts.

29 nation therapy was comparable to that of the isografts.

30 the HSP response in treated versus untreated isografts.

31 e majority of the few remaining monocytes in isografts.

32 sively in allografts but only transiently in isografts.

33 ative pathway of complement, in IRI to heart isografts.

34 Bcl-2 protein limits I/R injury in rat lung isografts.

35 y expressed in allografts when compared with isografts.

36 n in allografts and no signs of rejection in isografts.

37 were examined in small-bowel allografts and isografts.

38 d and interleukin-6 (IL-6)-treated steatotic isografts.

39 response between the parental tumor and its isografts.

40 shown to influence primary function of islet isografts.

41 ynthase (iNOS) protein in allografts but not isografts.

42 y use human tumor xenografts or murine tumor isografts.

43 thelial cells, and only IP-10 was induced by isografting.

44 eNG, rNG, and normal isografts (15 mm long) were implanted in the peroneal ne

45 4 with a ninefold increase as compared with isografts (24.0+/-3.7% vs. 2.7+/-0.5; P<0.05).

46 ontinuous hormone stimulation with pituitary isografts; (3) multiple pregnancies; (4) DMBA alone; and

47 antly higher hydroxyproline content than the isografts (33.21 +/- 1.89 versus 22.36 +/- 2.33 mug/mL).

48 ercentage of luminal occlusion compared with isografts (47% compared with 1.2%).

49 8+/-0.46 ml/min/kg) compared to nonrejecting isografts (7.98+/-1.62 ml/min/kg; P<0.01), but significa

50 c cells in DBA/2-->DBA/2 heterotopic cardiac isografts, acutely rejecting DBA/2-->C57BL/6 cardiac all

51 e intense nonimmune inflammation produced in isografts after donor BD may represent the initial stage

52 of 566+/-19, 76+/-22, and 504+/-105 mmHg for isograft, allograft, and aminoguanidine-treated allograf

53 Compared with airway isografts, allografts exhibited a significant increase i

54 ed native kidney; and Gp 4, those bearing an isograft and a sham-clipped native kidney.

55 terally nephrectomized LEW recipients as the isograft and allograft control, respectively.

56 Isograft and allograft controls received no treatment.

57 ted in normal eyes, remained unchanged among isograft and allograft groups.

58 Isograft and further allograft recipients were killed, a

59 controls--F-344 rats received an F-344 renal isograft and low-dose CsA; (3) experimental group--F-344

60 Isografts and 42.9% of allografts achieved normal clinic

61 Isografts and allografts (Fisher 344 rats-->LEW) from 45

62 , transient MIP-2 and MCP-1/JE production in isografts and allografts correlated with neutrophil and

63 ent, early MIP-2, and MCP-1/JE production in isografts and allografts correlated with neutrophil and

64 Vascular lesions of aortic isografts and allografts were evaluated quantitatively w

65 g-term effects of this risk factor on kidney isografts and allografts were examined with a rat model.

66 erence in HSP levels in cyclosporine-treated isografts and allografts.

67 anism of early PMN infiltration into cardiac isografts and allografts.

68 subcutaneous implantation of murine tracheal isografts and allografts.

69 as expressed at equivalent levels in C57BL/6 isografts and bm1 and bm12 allografts.

70 ina, muscle, kidney, and uvea) compared with isografts and controls.

71 ombined immunodeficient disease (SCID) islet isografts and delayed the rejection of allogeneic C57BL/

72 ED1+ cells were rare in isografts and did not stain for HO.

73 urvival following IRI in both Lewis-to-Lewis isografts and Fischer-to-Lewis allografts.

74 hanges were markedly less pronounced in Gp 3 isografts and minimal in the kidneys of the normotensive

75 Lewis isografts and normal Fischer-344 kidneys served as contr

76 2 and g = 1.94 (for Fe-S cluster protein) in isografts and normal hearts.

77 or functions of leukocytes in allografts and isografts and provide a foundation for testing their fun

78 into FN increases by day 1 in allografts and isografts and remains high until allografts are rejected

79 Lewis renal isografts and uninephrectomized rats that did not underg

80 .05 pmol L-citrulline.mg protein-1.min-1 for isografts) and was significantly reduced with dexamethas

81 ary blood flow ratio, the weight gain of the isograft, and the scores for histological categories of

82 issue from tolerant, acutely rejecting (AR), isografted, and naive animals using nonisotopic in situ

83 an Th2 cytokines in allografts compared with isografts, and both Th1 and Th2 cytokine gene expression

84 and 9 (45%) of 20 PRKO mice with a pituitary isograft; and (b) 10 (50%) of 20 WT mice and 10 (50%) of

85 14), cyclosporine-treated (10 mg/kg SQ/day) isografted animals (n = 12), and cyclosporine-treated al

86 raft and a sham-clipped native kidney; Gp 3, isografted animals with a clipped native kidney; and Gp

87 no histologic evidence of acute rejection in isografted animals.

88 entum of Lewis (allografts) or Brown Norway (isografts) animals.

89 ed tracheas obliterated completely, although isografts appeared patent with normal respiratory epithe

90 an additional group of mice receiving renal isografts as controls.

91 een in untreated allografts as compared with isografts as determined by PhosphorImage analysis.

92 control specimens and syngeneic transplants (isografts) as control specimens for the alloimmune respo

93 CS-1+ FNs increase in allografts and isografts at 3 hours after transplantation but are parti

94 ificantly greater than that of the untreated isografts at all time points.

95 in C57BL/6 allogeneic skin grafts and BALB/c isografts at day 2 posttransplant.

96 or each) in the allografts compared with the isografts at Weeks 2 through 6.

97 had received allografts; three had received isografts) at 7 T.

98 Isografts (BALB/c into BALB/c) and allografts (BALB/c in

99 Isografts (BALB/c into BALB/c) and allografts (BALB/c in

100 ssion was negligible in nonrejecting cardiac isografts but was significantly enhanced in rejecting al

101 ansplant, chemokine mRNA levels decreased in isografts but were maintained at high levels in the allo

102 No IL-10 was seen in isografts, but IL-4 was detected in 3/5 isografts.

103 bitor, prevents primary nonfunction of islet isografts by reducing inflammatory reactions at the graf

104 onged cold ischemia can initiate mild GAD in isografts by transiently enhancing antigen non-specific

105 , and epithelial cell replacement in denuded isografts can significantly reduce the fibrotic progress

106 y of murine heterotopic vascularized cardiac isografts caused a small, albeit significant, increase i

107 Relative to control isografts, cold ischemia induced transiently enhanced en

108 response to xenografts is sufficient to kill isografts complicates issues of immunoprotection, sugges

109 In contrast, isografts continued to beat beyond 90 days.

110 The isograft control was performed from LBN-F1 into LBN-F1.

111 (standard uptake value allograft, 2.8+/-0.3; isograft control, 1.7+/-0.2; P<0.05).

112 e untreated allograft in comparison with the isograft control, of which 77 genes were categorized as

113 All isograft controls (Lewis to Lewis, n=6) survived unevent

114 As references, we used 55-day isograft controls (n=5) and native hearts (n=6).

115 ls demonstrated severe parenchymal fibrosis; isograft controls and intrathymic (IT) animals failed to

116 e in allograft controls and were absent from isograft controls and IT allografts as determined by rev

117 sed to approximately 50% of that observed in isograft controls by POD4.

118 grafts with chronic vasculopathy compared to isograft controls on day 28 (P = 0.01).

119 Isograft controls survived indefinitely.

120 Isograft controls survived indefinitely; in allografts w

121 In allograft recipients and isograft controls, NF-kappaB was assayed by electrophore

122 10 days of low-dose cyclosporine (CsA); (2) isograft controls--F-344 rats received an F-344 renal is

123 nor hearts into C57BL/6 recipients served as isograft controls.

124 and 28 (4.8% vs 0.9%; P = 0.006) compared to isograft controls.

125 ays) but falls to normal levels in tolerated isografts (day 6).

126 Isografts demonstrated normal histology with minimal HO-

127 LEW and DA recipients of liver isografts developed no toxicity and survived indefinitel

128 Isografts did not display the late pattern of sustained

129 Rejecting allografts and isografts did not express intragraft IL-10.

130 Donor hearts and isografts did not express myocardial VSM alpha-actin, in

131 (1) Cardiac isografts display no detectable TUNEL+ cells.

132 6 pretreatment of steatotic Zucker rat liver isografts dramatically reduces mortality and liver injur

133 Isografts, eNG, and rNG all had similar patterns of pero

134 Treatment of islet isografts ex vivo with ad5-CMV-beta-galactosidase result

135 exhibited decreased ADC values (P <.01) and isografts exhibited similar ADC values compared with nat

136 nd active TGF-beta, whereas accepted cardiac isografts express only tPA, but not uPA or activated TGF

137 The isografts expressed more epidermal growth factor than al

138 Isograft expression of RANTES and IP-10 was undetectable

139 expressed at equivalent levels in allo- and isografts for 2-4 days posttransplant and then returned

140 METHODS AND We transplanted isografts from B6 mice and allografts from Balb/c mice h

141 r, and molecular changes occurring in kidney isografts from BD donors are compared with those from no

142 At 5 days, the isografts from BD donors were highly infiltrated by host

143 Changes in isografts from brain-dead donors were less marked and de

144 Arterial isografts from donor WT mice that had been anastamosed t

145 Groups included both allografts and isografts from normotensive brain dead donors and anesth

146 Histological examination of islet isografts from these rats showed complete destruction of

147 Bone marrow (BM) isografts from WKY to WKY or Lewis to Lewis did not affe

148 CCL2 inversely correlated (P < 0.0001) with isograft function.

149 Isografts generally showed no arterial changes.

150 Isograft glomerular filtration rate (GFR) was measured a

151 ses of 55% and 97% above the activity in the isografted group in hepatic uptake of annexin V on days

152 ation was detected between the xenograft and isograft groups.

153 e found that most normal tissues and cardiac isografts had minimal expression of PD-1, PD-L1, or PD-L

154 All isografts had normal function.

155 Mouse heterotopic isograft heart transplants were performed in C57BL/6 mic

156 f vimentin preimmunization on allogeneic and isografted hearts in a murine transplant model.

157 ll adhesion molecule-1 compared to normal or isografted hearts.

158 rafted (immunologically mismatched) and five isografted (immunologically matched) recipient rats on d

159 ET-1 levels increase after isograft implantation, and ET-1 plays a key role in CNI-

160 Utilizing small intestine isografts implanted into the subcutaneous tissue of adul

161 xenografts and allografts in comparison with isografts in diffusion chambers with 0.4-microm pore mem

162 rence of diabetes in renal subcapsular islet isografts in DR-BB (RT1uu) rats with established autoimm

163 , and the latter were indistinguishable from isografts in either WT or SCID recipients, indicating a

164 revented the recurrence of diabetes in islet isografts in rats with established autoimmune diabetes.

165 f in situ administration of this agent on FP isografts in rats.

166 for preservation-reperfusion injury of lung isografts in the rat.

167 factors was locally administered to eight FP isografts in the thigh muscle of diabetic rats.

168 Immunofluorescent staining of islet isografts infected with ad5-CMV-beta-galactosidase revea

169 Mononuclear cells recirculated to native and isografted intestine and recirculation was inhibited by

170 Isografted intestine developed normally; it was not expo

171 The kidneys were then isografted into genetically identical Lewis rats and GFR

172 When a vein fragment from TIE2-LacZ was isografted into the carotid artery of wild-type mice, th

173 e of vein segments donated by wild-type mice isografted into TIE2-LacZ mice at 1 week and reached con

174 ing heparan sulfate phenotype in control and isografted kidneys toward a FGF2-binding phenotype in al

175 There were 4 experimental groups: untreated isografted (LEW to LEW) animals (n = 14), untreated allo

176 at I-FABP was not detectable in the serum of isografted Lewis rats, but could be measured in the peri

177 idney to a Lewis rat; n = 17) and in control isografts (Lewis kidney to a Lewis rat; n = 17).

178 was performed in histocompatibility matched (isografts: Lewis --> Lewis) and mismatched (allografts:

179 Kidney isografts (male Lewis rats [LEW]-->LEW) were transplante

180 In the absence of a pituitary isograft, mammary tumors developed in 4 (20%) of 20 WT m

181 ignificant vascular changes were observed in isografts (mean medial areas of 3.3 +/- 0.3x0(5) microm2

182 -dimethylbenz(a)anthracene (DMBA), pituitary-isografted mice, there was a marked reduction in mammary

183 bition of TLR2 promotes graft function in an isograft model of renal transplantation.

184 An isograft model was used to demonstrate that retrieval an

185 lung preservation and transplantation in an isograft model, and that inhibiting complement activatio

186 nfirming local complement activation in this isograft model.

187 mus (Tac) and sirolimus (Sir) in a rat renal isograft model.

188 ects of Ad-HO-1 gene transfer in a rat renal isograft model.

189 tumour progression in multiple subcutaneous isograft models and an autochthonous transgenic model of

190 an resting membrane potential of control and isograft muscle cells was -69 +/- 0.9 mV with a slow-wav

191 survival times of tobacco-treated animals), isografts (n=3), both donor and recipient rats exposed t

192 0 mg/kg per day by oral gavage, n = 10), and isograft negative control (Lewis-to-Lewis, n = 5).

193 DBA/2-->DBA/2 cardiac isografts never displayed TVS in this time period, but d

194 The isograft not only developed into a morphologically norma

195 Controls included allografts and isografts not treated with CsA.

196 In aortic isografts of apolipoprotein E-knockout mice treated with

197 Isografts of either PDK1- or PKCalpha-expressing cells b

198 In contrast, vascular changes in isografts of hypertensive hosts were restricted to media

199 rats were given an eNG on the right, and an isograft on the left.

200 ted signal in rejected allografts but not in isografts or MPO-deficient allograft recipients.

201 ry cytokine genes was not observed in either isografts or native heart.

202 eas no staining was detectable in WKY to WKY isografts or native lungs.

203 /c, H-2L(d+)) were transplanted into BALB/c (isografts), or single class I MHC-mismatched (L(d)-defic

204 d severe acute rejection, but not in normal, isograft, or allograft lungs before histological changes

205 erved in FK506-treated allograft recipients, isografts, or native intestine of allograft recipients.

206 s 3.2 +/- 0.5 versus 1.1 +/- 0.4 in diabetic isografts (P < 0.03) and zero TxCAD in nondiabetic allog

207 tor (A2AR) in WT allografts compared with WT isografts (p = 0.032), additional experiments were perfo

208 3 +/- 2% luminal occlusion vs. 17 +/- 1% for isografts, P < 0.05) with sites of obstructive lesion fo

209 levels (67 +/- 5 versus 18 +/- 2 microM for isografts; P < 0.001) that were significantly reduced by

210 In this study, we isografted PanO2 pancreatic carcinoma cells into mice in

211 PMN infiltration into isografts peaked at 9 to 12 hours post-transplant and qu

212 C3-/- kidney isografts placed in wild-type C3+/+ mice were protected

213 2 resulted in reduced PIP and increased lung isograft pulmonary vein PaO(2) compared with AdvNull or

214 Twenty-one allograft (PVG.1U-->PVG.R8) and 9 isograft (PVG.R8-->PVG.R8) transplantations were perform

215 al were superior to irradiated allograft and isograft rates of survival (P < 0.001).

216 Nonirradiated allograft and isograft rates of survival were superior to irradiated a

217 Isograft rats (n=5) and control allograft rats (n=4) rec

218 Early survival and renal dysfunction of isografted rats correlated with the interval of donor ca

219 ere associated with sutures in allograft and isograft recipients and within conjunctivae, either scat

220 immune rats were transferred to WKY rat lung isograft recipients followed by assessments of lung path

221 significantly higher than the BP of control isograft recipients.

222 more severe in bm1 and F1 allografts than in isografts recovered from B6 recipients, but bm12 allogra

223 ssion of these genes in nonrejecting cardiac isografts, rejecting cardiac allografts, and cardiac all

224 Isografts remained functional for >100 days, whereas all

225 ant models using wild-type animals, tracheal isografts remained open without rejection, whereas allog

226 Islet isografts removed from the rats showed low levels of ins

227 Isografts resisted LCMV-induced rejection, and the inter

228 Isograft retransplantation resulted in a similar inciden

229 Miller staining of the isografts revealed disruption of the basement membrane a

230 In a guinea pig-to-guinea pig (n=6) isograft series, biopsy controls for preservation/ischem

231 anted into C57BL/6 (B6, H-2b) recipients; B6 isografts served as controls.

232 Untreated Lewis to Lewis isografts served as histological controls.

233 In contrast, day-90 cardiac isografts showed little to no TVS development.

234 ACI isografts showed no evidence of CGVD (n=6) at day 90.

235 In isografts, stable luminescence intensity signals occurre

236 ibit alveologenesis in response to pituitary isograft stimulation; thus, DMBA-initiated mammary tumor

237 In addition, 90% of the rats receiving liver isografts stored in UW solution supplemented with PSGL-1

238 jection were absent in long-term transfected isografts, suggesting that long-term expression of activ

239 determine the effect of selectin blockade on isograft survival in a syngeneic rat orthotopic liver tr

240 ocumented by a significant increase in liver isograft survival.

241 Isografts survived >30 days regardless of OVA(323-339) a

242 Ifnb-/- mice with intracerebral isografts survived poorly.

243 0(-6)) were 2- to 10-fold higher compared to isografts throughout the time-course of graft injury.

244 ograft animals when compared with normal and isograft tissues.

245 nimals when compared with that in normal and isograft tissues.

246 ued by allowing embryonic Fiaf-/- intestinal isografts to develop in Fiaf+/+ recipients.

247 at transgene expression persisted in cardiac isografts transfected with an adenovirus encoding beta-g

248 After isograft transplantation, weight bearing began by day 17

249 ctional in vivo cross talk in the setting of isograft transplantation.

250 The composite hemiface isograft transplantations were performed in group 1.

251 s (blood glucose > 300 mg/dl) received 16 FP isografts transplanted intramuscularly.

252 Isograft transplants (Lewis to Lewis, +DM/+/-F) were con

253 Isograft transplants survived indefinitely.

254 ermore, growth of highly aggressive melanoma isograft tumors was suppressed by single agent treatment

255 ary gland grafts by inclusion of a pituitary isograft under the renal capsule as a source of prolacti

256 Mild GAD developed in isografts undergoing 4-hour cold ischemia.

257 and 50 days (group 3) and compared with F344 isografts undergoing retransplantation after 4 days (gro

258 opment of coronary lesions in retransplanted isografts underlines the participation of antigen-indepe

259 NA expression remains nearly constant in the isograft, unlike the normal intact small intestine.

260 Recipients underwent left nephrectomy and isografting using standard techniques.

261 ion by illuminating intraperitoneally placed isografts using a laparotomy.

262 XCL10 on the autoimmune destruction of islet isografts using RIP-LCMV mice expressing a lymphocytic c

263 gher protease activity in allografts than in isografts using tomographic fluorescence.

264 ed allograft serum nitrite/nitrate levels to isograft values.

265 severe atherosclerosis and vessel rupture in isografted vessels of apolipoprotein E-knockout mice occ

266 induces hepatoprotection of steatotic liver isografts via preventing sinusoidal endothelial cell nec

267 am operation was used as the control and the isograft was used as the benchmark procedure.

268 Expression of these genes in control isografts was at low levels, with the exception of JE, w

269 Class II expression in isografts was limited to epicardial macrophages.

270 Expression of IP-10 and Mig in isografts was low or undetectable.

271 immune destruction of CXCL10-deficient islet isografts was significantly reduced.

272 Using murine isografts, we attempted to prevent this islet graft dama

273 Small portions of the lung isograft were excised and stained with an antibody speci

274 By contrast, pituitary isografts were able to rescue the ductal elongation phen

275 Isografts were analyzed 48 hours after transplantation f

276 Lung isografts were analyzed using micro-positron emission to

277 inferior vena cava-to-carotid interposition isografts were completed using an anastomotic cuff techn

278 Rat trachea isografts were denuded of epithelium by protease digesti

279 Lung isografts were injured and platelets accumulated in the

280 Heterotopic brown Norway rat cardiac isografts were removed on postoperative day (POD) 3, 5,

281 Treated animals and isografts were sacrificed 120-130 days posttransplant fo

282 BALB/c allografts and C57BL/6 (B6) isografts were transplanted into B6 severe combined immu

283 Immunohistochemistry and murine intestinal isografts were used in which the small intestine from ne

284 sufficient to induce rejection pathology in isografts, whereas tolerance to col(V) suppresses allogr

285 necrapoptosis in steatotic Zucker rat liver isografts, which is prevented by in vitro IL-6 pretreatm

286 th WF cells, unlike lymphocytes from the LEW isografts, which produced Th1 cytokines when challenged

287 ograft without immunosuppression, n=7), III (isograft with immunosuppression, n=5), and IV (isograft

288 tion of the insulin-producing portion of the isograft with residual cells positive for glucagon.

289 Treatment of fetal pancreas (FP) isografts with insulin-like growth factor-I greatly impr

290 (4/9) allografts were indistinguishable from isografts with no evidence of rejection, and were consid

291 hormones, and virgin mice bearing pituitary isografts with persistently elevated hormones.

292 ografts showed inferior survival compared to isografts, with no difference in survival between the al

293 ograft with immunosuppression, n=5), and IV (isograft without immunosuppression, n=6) were included t

294 ntation after 4 days (group 4) and with F344 isografts without a second procedure (group 5).

295 37 +/- 9%, NS), whereas coronary arteries of isografts without a second transplant procedure (group 5

296 bronchiolar and perivascular inflammation in isograft (WKY) lungs and abrogated col(V)-induced oral t