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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  polymorphonuclear leukocyte influx into the isograft.
5 otec on the individual tissues of a rat limb isograft.
6 n in allografts and no signs of rejection in isografts.
7 y use human tumor xenografts or murine tumor isografts.
8 were significantly decreased in transplanted isografts.
9 ng growth factor-beta in these cold-ischemic isografts.
10 re tested for their ability to reject second isografts.
11 ifferences between control and cold ischemic isografts.
12 M-1 and cytokines comparable to that seen in isografts.
13 own in both transfected COS7 cells and heart isografts.
14  infiltration was greater in allografts than isografts.
15                  Group 4 rats (n=3) received isografts.
16 cies; (4) DMBA alone; and (5) DMBA+pituitary isografts.
17 n in isografts, but IL-4 was detected in 3/5 isografts.
18 mpared with acutely rejecting allografts and isografts.
19 t bm12 allografts appeared no different than isografts.
20 titate the intensity of antibody staining in isografts.
21 ee in the immediately adjacent myocardium in isografts.
22 ion after 18-h culture than cells from liver isografts.
23 challenge, allografts, or without challenge, isografts.
24 l as in intimal thickness when compared with isografts.
25    EIIIB+ FN ratios remain relatively low in isografts.
26 nhance nerve regeneration in the same way as isografts.
27 irway lumen, changes not seen in heterotopic isografts.
28 ected into the rNG and the resident cells of isografts.
29 nation therapy was comparable to that of the isografts.
30 DBA/2 kidneys or B6.Foxp3(DTR) recipients of isografts.
31 the HSP response in treated versus untreated isografts.
32 in the cellular infiltrates around the islet isografts.
33 e majority of the few remaining monocytes in isografts.
34 sively in allografts but only transiently in isografts.
35 ative pathway of complement, in IRI to heart isografts.
36  Bcl-2 protein limits I/R injury in rat lung isografts.
37 y expressed in allografts when compared with isografts.
38  were examined in small-bowel allografts and isografts.
39 d and interleukin-6 (IL-6)-treated steatotic isografts.
40  response between the parental tumor and its isografts.
41 shown to influence primary function of islet isografts.
42 ynthase (iNOS) protein in allografts but not 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 ly twofold longer survival in an orthotopic, isograft breast cancer mouse model.
101 ssion was negligible in nonrejecting cardiac isografts but was significantly enhanced in rejecting al
102 ansplant, chemokine mRNA levels decreased in isografts but were maintained at high levels in the allo
103                         No IL-10 was seen in isografts, but IL-4 was detected in 3/5 isografts.
104 bitor, prevents primary nonfunction of islet isografts by reducing inflammatory reactions at the graf
105 onged cold ischemia can initiate mild GAD in isografts by transiently enhancing antigen non-specific
106 , and epithelial cell replacement in denuded isografts can significantly reduce the fibrotic progress
107 y of murine heterotopic vascularized cardiac isografts caused a small, albeit significant, increase i
108                          Relative to control isografts, cold ischemia induced transiently enhanced en
109 response to xenografts is sufficient to kill isografts complicates issues of immunoprotection, sugges
110                                 In contrast, isografts continued to beat beyond 90 days.
111                                          The isograft control was performed from LBN-F1 into LBN-F1.
112 (standard uptake value allograft, 2.8+/-0.3; isograft control, 1.7+/-0.2; P<0.05).
113 e untreated allograft in comparison with the isograft control, of which 77 genes were categorized as
114                                          All isograft controls (Lewis to Lewis, n=6) survived unevent
115                As references, we used 55-day isograft controls (n=5) and native hearts (n=6).
116 ls demonstrated severe parenchymal fibrosis; isograft controls and intrathymic (IT) animals failed to
117 e in allograft controls and were absent from isograft controls and IT allografts as determined by rev
118 sed to approximately 50% of that observed in isograft controls by POD4.
119 grafts with chronic vasculopathy compared to isograft controls on day 28 (P = 0.01).
120                                              Isograft controls survived indefinitely.
121                                              Isograft controls survived indefinitely; in allografts w
122                  In allograft recipients and isograft controls, NF-kappaB was assayed by electrophore
123  10 days of low-dose cyclosporine (CsA); (2) isograft controls--F-344 rats received an F-344 renal is
124 nor hearts into C57BL/6 recipients served as isograft controls.
125 and 28 (4.8% vs 0.9%; P = 0.006) compared to isograft controls.
126 ays) but falls to normal levels in tolerated isografts (day 6).
127                                              Isografts demonstrated normal histology with minimal HO-
128 fter receiving a kidney allograft but not an isograft, despite the avoidance of antibiotics and immun
129               LEW and DA recipients of liver isografts developed no toxicity and survived indefinitel
130                                              Isografts did not display the late pattern of sustained
131                     Rejecting allografts and isografts did not express intragraft IL-10.
132                             Donor hearts and isografts did not express myocardial VSM alpha-actin, in
133                                  (1) Cardiac isografts display no detectable TUNEL+ cells.
134 6 pretreatment of steatotic Zucker rat liver isografts dramatically reduces mortality and liver injur
135                                              Isografts, eNG, and rNG all had similar patterns of pero
136                           Treatment of islet isografts ex vivo with ad5-CMV-beta-galactosidase result
137  exhibited decreased ADC values (P <.01) and isografts exhibited similar ADC values compared with nat
138 nd active TGF-beta, whereas accepted cardiac isografts express only tPA, but not uPA or activated TGF
139                                          The isografts expressed more epidermal growth factor than al
140                                              Isograft expression of RANTES and IP-10 was undetectable
141  expressed at equivalent levels in allo- and isografts for 2-4 days posttransplant and then returned
142                  METHODS AND We transplanted isografts from B6 mice and allografts from Balb/c mice h
143 r, and molecular changes occurring in kidney isografts from BD donors are compared with those from no
144                               At 5 days, the isografts from BD donors were highly infiltrated by host
145                                   Changes in isografts from brain-dead donors were less marked and de
146                                     Arterial isografts from donor WT mice that had been anastamosed t
147          Groups included both allografts and isografts from normotensive brain dead donors and anesth
148            Histological examination of islet isografts from these rats showed complete destruction of
149                             Bone marrow (BM) isografts from WKY to WKY or Lewis to Lewis did not affe
150  CCL2 inversely correlated (P < 0.0001) with isograft function.
151                                              Isografts generally showed no arterial changes.
152                                              Isograft glomerular filtration rate (GFR) was measured a
153 ses of 55% and 97% above the activity in the isografted group in hepatic uptake of annexin V on days
154 ation was detected between the xenograft and isograft groups.
155 e found that most normal tissues and cardiac isografts had minimal expression of PD-1, PD-L1, or PD-L
156                                          All isografts had normal function.
157                            Mouse heterotopic isograft heart transplants were performed in C57BL/6 mic
158 f vimentin preimmunization on allogeneic and isografted hearts in a murine transplant model.
159 ll adhesion molecule-1 compared to normal or isografted hearts.
160 rafted (immunologically mismatched) and five isografted (immunologically matched) recipient rats on d
161                   ET-1 levels increase after isograft implantation, and ET-1 plays a key role in CNI-
162                    Utilizing small intestine isografts implanted into the subcutaneous tissue of adul
163 xenografts and allografts in comparison with isografts in diffusion chambers with 0.4-microm pore mem
164 rence of diabetes in renal subcapsular islet isografts in DR-BB (RT1uu) rats with established autoimm
165 , and the latter were indistinguishable from isografts in either WT or SCID recipients, indicating a
166 revented the recurrence of diabetes in islet isografts in rats with established autoimmune diabetes.
167 f in situ administration of this agent on FP isografts in rats.
168  for preservation-reperfusion injury of lung isografts in the rat.
169 factors was locally administered to eight FP isografts in the thigh muscle of diabetic rats.
170          Immunofluorescent staining of islet isografts infected with ad5-CMV-beta-galactosidase revea
171 Mononuclear cells recirculated to native and isografted intestine and recirculation was inhibited by
172                                              Isografted intestine developed normally; it was not expo
173                        The kidneys were then isografted into genetically identical Lewis rats and GFR
174      When a vein fragment from TIE2-LacZ was isografted into the carotid artery of wild-type mice, th
175 e of vein segments donated by wild-type mice isografted into TIE2-LacZ mice at 1 week and reached con
176 ing heparan sulfate phenotype in control and isografted kidneys toward a FGF2-binding phenotype in al
177  There were 4 experimental groups: untreated isografted (LEW to LEW) animals (n = 14), untreated allo
178 at I-FABP was not detectable in the serum of isografted Lewis rats, but could be measured in the peri
179 idney to a Lewis rat; n = 17) and in control isografts (Lewis kidney to a Lewis rat; n = 17).
180 was performed in histocompatibility matched (isografts: Lewis --> Lewis) and mismatched (allografts:
181                                              Isografts maintained good oxygenation and perfusion thro
182                                       Kidney isografts (male Lewis rats [LEW]-->LEW) were transplante
183                In the absence of a pituitary isograft, mammary tumors developed in 4 (20%) of 20 WT m
184 ignificant vascular changes were observed in isografts (mean medial areas of 3.3 +/- 0.3x0(5) microm2
185 -dimethylbenz(a)anthracene (DMBA), pituitary-isografted mice, there was a marked reduction in mammary
186 bition of TLR2 promotes graft function in an isograft model of renal transplantation.
187                                           An isograft model was used to demonstrate that retrieval an
188  lung preservation and transplantation in an isograft model, and that inhibiting complement activatio
189 nfirming local complement activation in this isograft model.
190 mus (Tac) and sirolimus (Sir) in a rat renal isograft model.
191 ects of Ad-HO-1 gene transfer in a rat renal isograft model.
192  tumour progression in multiple subcutaneous isograft models and an autochthonous transgenic model of
193             Here, we established an arterial isograft mouse model in wild-type and endothelial RIPK1
194 an resting membrane potential of control and isograft muscle cells was -69 +/- 0.9 mV with a slow-wav
195  survival times of tobacco-treated animals), isografts (n=3), both donor and recipient rats exposed t
196 0 mg/kg per day by oral gavage, n = 10), and isograft negative control (Lewis-to-Lewis, n = 5).
197                        DBA/2-->DBA/2 cardiac isografts never displayed TVS in this time period, but d
198                                          The isograft not only developed into a morphologically norma
199             Controls included allografts and isografts not treated with CsA.
200                                    In aortic isografts of apolipoprotein E-knockout mice treated with
201                                              Isografts of either PDK1- or PKCalpha-expressing cells b
202             In contrast, vascular changes in isografts of hypertensive hosts were restricted to media
203  rats were given an eNG on the right, and an isograft on the left.
204 ted signal in rejected allografts but not in isografts or MPO-deficient allograft recipients.
205 ry cytokine genes was not observed in either isografts or native heart.
206 eas no staining was detectable in WKY to WKY isografts or native lungs.
207 /c, H-2L(d+)) were transplanted into BALB/c (isografts), or single class I MHC-mismatched (L(d)-defic
208 d severe acute rejection, but not in normal, isograft, or allograft lungs before histological changes
209 erved in FK506-treated allograft recipients, isografts, or native intestine of allograft recipients.
210 s 3.2 +/- 0.5 versus 1.1 +/- 0.4 in diabetic isografts (P < 0.03) and zero TxCAD in nondiabetic allog
211 tor (A2AR) in WT allografts compared with WT isografts (p = 0.032), additional experiments were perfo
212 3 +/- 2% luminal occlusion vs. 17 +/- 1% for isografts, P < 0.05) with sites of obstructive lesion fo
213  levels (67 +/- 5 versus 18 +/- 2 microM for isografts; P < 0.001) that were significantly reduced by
214                            In this study, we isografted PanO2 pancreatic carcinoma cells into mice in
215                        PMN infiltration into isografts peaked at 9 to 12 hours post-transplant and qu
216                                 C3-/- kidney isografts placed in wild-type C3+/+ mice were protected
217 2 resulted in reduced PIP and increased lung isograft pulmonary vein PaO(2) compared with AdvNull or
218 Twenty-one allograft (PVG.1U-->PVG.R8) and 9 isograft (PVG.R8-->PVG.R8) transplantations were perform
219 al were superior to irradiated allograft and isograft rates of survival (P < 0.001).
220                  Nonirradiated allograft and isograft rates of survival were superior to irradiated a
221                                              Isograft rats (n=5) and control allograft rats (n=4) rec
222      Early survival and renal dysfunction of isografted rats correlated with the interval of donor ca
223 ere associated with sutures in allograft and isograft recipients and within conjunctivae, either scat
224 immune rats were transferred to WKY rat lung isograft recipients followed by assessments of lung path
225  significantly higher than the BP of control isograft recipients.
226 more severe in bm1 and F1 allografts than in isografts recovered from B6 recipients, but bm12 allogra
227 ssion of these genes in nonrejecting cardiac isografts, rejecting cardiac allografts, and cardiac all
228                                              Isografts remained functional for >100 days, whereas all
229 ant models using wild-type animals, tracheal isografts remained open without rejection, whereas allog
230                                        Islet isografts removed from the rats showed low levels of ins
231                                              Isografts resisted LCMV-induced rejection, and the inter
232                                              Isograft retransplantation resulted in a similar inciden
233                       Miller staining of the isografts revealed disruption of the basement membrane a
234          In a guinea pig-to-guinea pig (n=6) isograft series, biopsy controls for preservation/ischem
235 anted into C57BL/6 (B6, H-2b) recipients; B6 isografts served as controls.
236                     Untreated Lewis to Lewis isografts served as histological controls.
237                  In contrast, day-90 cardiac isografts showed little to no TVS development.
238                                          ACI isografts showed no evidence of CGVD (n=6) at day 90.
239                                           In isografts, stable luminescence intensity signals occurre
240 ibit alveologenesis in response to pituitary isograft stimulation; thus, DMBA-initiated mammary tumor
241 In addition, 90% of the rats receiving liver isografts stored in UW solution supplemented with PSGL-1
242 jection were absent in long-term transfected isografts, suggesting that long-term expression of activ
243 determine the effect of selectin blockade on isograft survival in a syngeneic rat orthotopic liver tr
244 ocumented by a significant increase in liver isograft survival.
245                                              Isografts survived >30 days regardless of OVA(323-339) a
246              Ifnb-/- mice with intracerebral isografts survived poorly.
247 0(-6)) were 2- to 10-fold higher compared to isografts throughout the time-course of graft injury.
248 ograft animals when compared with normal and isograft tissues.
249 nimals when compared with that in normal and isograft tissues.
250 ued by allowing embryonic Fiaf-/- intestinal isografts to develop in Fiaf+/+ recipients.
251 at transgene expression persisted in cardiac isografts transfected with an adenovirus encoding beta-g
252                                        After isograft transplantation, weight bearing began by day 17
253 ctional in vivo cross talk in the setting of isograft transplantation.
254                       The composite hemiface isograft transplantations were performed in group 1.
255 s (blood glucose > 300 mg/dl) received 16 FP isografts transplanted intramuscularly.
256                                              Isograft transplants (Lewis to Lewis, +DM/+/-F) were con
257                                              Isograft transplants survived indefinitely.
258 ermore, growth of highly aggressive melanoma isograft tumors was suppressed by single agent treatment
259 ary gland grafts by inclusion of a pituitary isograft under the renal capsule as a source of prolacti
260                        Mild GAD developed in isografts undergoing 4-hour cold ischemia.
261 and 50 days (group 3) and compared with F344 isografts undergoing retransplantation after 4 days (gro
262 opment of coronary lesions in retransplanted isografts underlines the participation of antigen-indepe
263 NA expression remains nearly constant in the isograft, unlike the normal intact small intestine.
264    Recipients underwent left nephrectomy and isografting using standard techniques.
265 ion by illuminating intraperitoneally placed isografts using a laparotomy.
266 XCL10 on the autoimmune destruction of islet isografts using RIP-LCMV mice expressing a lymphocytic c
267 gher protease activity in allografts than in isografts using tomographic fluorescence.
268 ed allograft serum nitrite/nitrate levels to isograft values.
269 severe atherosclerosis and vessel rupture in isografted vessels of apolipoprotein E-knockout mice occ
270  induces hepatoprotection of steatotic liver isografts via preventing sinusoidal endothelial cell nec
271 am operation was used as the control and the isograft was used as the benchmark procedure.
272         Expression of these genes in control isografts was at low levels, with the exception of JE, w
273                       Class II expression in isografts was limited to epicardial macrophages.
274               Expression of IP-10 and Mig in isografts was low or undetectable.
275 immune destruction of CXCL10-deficient islet isografts was significantly reduced.
276                                 Using murine isografts, we attempted to prevent this islet graft dama
277                   Small portions of the lung isograft were excised and stained with an antibody speci
278                       By contrast, pituitary isografts were able to rescue the ductal elongation phen
279                                              Isografts were analyzed 48 hours after transplantation f
280                                         Lung isografts were analyzed using micro-positron emission to
281  inferior vena cava-to-carotid interposition isografts were completed using an anastomotic cuff techn
282                                  Rat trachea isografts were denuded of epithelium by protease digesti
283                                         Lung isografts were injured and platelets accumulated in the
284         Heterotopic brown Norway rat cardiac isografts were removed on postoperative day (POD) 3, 5,
285                          Treated animals and isografts were sacrificed 120-130 days posttransplant fo
286           BALB/c allografts and C57BL/6 (B6) isografts were transplanted into B6 severe combined immu
287   Immunohistochemistry and murine intestinal isografts were used in which the small intestine from ne
288  sufficient to induce rejection pathology in isografts, whereas tolerance to col(V) suppresses allogr
289  necrapoptosis in steatotic Zucker rat liver isografts, which is prevented by in vitro IL-6 pretreatm
290 th WF cells, unlike lymphocytes from the LEW isografts, which produced Th1 cytokines when challenged
291 ograft without immunosuppression, n=7), III (isograft with immunosuppression, n=5), and IV (isograft
292 tion of the insulin-producing portion of the isograft with residual cells positive for glucagon.
293             Treatment of fetal pancreas (FP) isografts with insulin-like growth factor-I greatly impr
294 (4/9) allografts were indistinguishable from isografts with no evidence of rejection, and were consid
295  hormones, and virgin mice bearing pituitary isografts with persistently elevated hormones.
296 ografts showed inferior survival compared to isografts, with no difference in survival between the al
297 ograft with immunosuppression, n=5), and IV (isograft without immunosuppression, n=6) were included t
298 ntation after 4 days (group 4) and with F344 isografts without a second procedure (group 5).
299 37 +/- 9%, NS), whereas coronary arteries of isografts without a second transplant procedure (group 5
300 bronchiolar and perivascular inflammation in isograft (WKY) lungs and abrogated col(V)-induced oral t

 
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