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PMID |
Sentence |
1 |
3825155
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The outcome of 532 femoro-popliteal vein grafts performed electively during the years 1970 to 1985 for obliterative arterial disease, was analyzed using the documentation-system of the Austrian Society for Vascular Surgery, as well as SAS and BMDP-software on an IBM 4381 computer of the Medical Faculty.
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2 |
8410734
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The data were analyzed with SAS and BMDP computer packages.
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3 |
9600104
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MRX could be formed by incubation of bovine serum albumin with glucose, followed by acid hydrolysis.
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4 |
10384512
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The same method is, in principle, applicable to patients of other diseases, too, using statistical software such as SAS, BMDP and etc.
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5 |
12054520
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Nestin-positive progenitor cells derived from adult human pancreatic islets of Langerhans contain side population (SP) cells defined by expression of the ABCG2 (BCRP1) ATP-binding cassette transporter.
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6 |
12054520
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Recently it was shown that the exclusion of the Hoechst 33342 dye, which defines the pluripotential side population (SP) of hematopoietic stem cells, is mediated by the ATP-binding cassette transporter, ABCG2.
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7 |
12054520
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Here we report that the human islet-derived NIPs contain a substantial subpopulation of SP cells that co-express ABCG2, MDR1, and nestin.
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8 |
12054520
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Nestin-positive progenitor cells derived from adult human pancreatic islets of Langerhans contain side population (SP) cells defined by expression of the ABCG2 (BCRP1) ATP-binding cassette transporter.
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9 |
12054520
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Recently it was shown that the exclusion of the Hoechst 33342 dye, which defines the pluripotential side population (SP) of hematopoietic stem cells, is mediated by the ATP-binding cassette transporter, ABCG2.
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10 |
12054520
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Here we report that the human islet-derived NIPs contain a substantial subpopulation of SP cells that co-express ABCG2, MDR1, and nestin.
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11 |
12054520
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Nestin-positive progenitor cells derived from adult human pancreatic islets of Langerhans contain side population (SP) cells defined by expression of the ABCG2 (BCRP1) ATP-binding cassette transporter.
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12 |
12054520
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Recently it was shown that the exclusion of the Hoechst 33342 dye, which defines the pluripotential side population (SP) of hematopoietic stem cells, is mediated by the ATP-binding cassette transporter, ABCG2.
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13 |
12054520
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Here we report that the human islet-derived NIPs contain a substantial subpopulation of SP cells that co-express ABCG2, MDR1, and nestin.
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14 |
12695557
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In the present study, we isolated and cultured human fetal NIPs that express stem cell marker ABCG2/BCRP1.
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15 |
12695557
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During differentiation, NIP-derived ICCs showed numerous pancreatic lineage transcripts including insulin, whereas ABCG2 and nestin expression fell concomitantly.
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16 |
12695557
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In the present study, we isolated and cultured human fetal NIPs that express stem cell marker ABCG2/BCRP1.
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17 |
12695557
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During differentiation, NIP-derived ICCs showed numerous pancreatic lineage transcripts including insulin, whereas ABCG2 and nestin expression fell concomitantly.
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18 |
16460677
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Human adipose tissue-derived mesenchymal stem cells differentiate into insulin, somatostatin, and glucagon expressing cells.
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19 |
16460677
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During the proliferation period, the cells expressed the stem cell markers nestin, ABCG2, SCF, Thy-1 as well as the pancreatic endocrine transcription factor Isl-1.
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20 |
16460677
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Using quantitative PCR a down-regulation of ABCG2 and up-regulation of pancreatic developmental transcription factors Isl-1, Ipf-1, and Ngn3 were observed together with induction of the islet hormones insulin, glucagon, and somatostatin.
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21 |
16460677
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Human adipose tissue-derived mesenchymal stem cells differentiate into insulin, somatostatin, and glucagon expressing cells.
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22 |
16460677
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During the proliferation period, the cells expressed the stem cell markers nestin, ABCG2, SCF, Thy-1 as well as the pancreatic endocrine transcription factor Isl-1.
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23 |
16460677
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Using quantitative PCR a down-regulation of ABCG2 and up-regulation of pancreatic developmental transcription factors Isl-1, Ipf-1, and Ngn3 were observed together with induction of the islet hormones insulin, glucagon, and somatostatin.
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24 |
17328838
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Here we report that CXCR4-positive pancreatic cells express markers of pancreatic endocrine progenitors (neurogenin-3, nestin) and markers of pluripotent stem cells (Oct-4, Nanog, ABCG2, CD133, CD117).
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25 |
17915193
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Insulin treatment may attenuate the impairment of Bcrp expression and function induced by diabetes.
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26 |
17915193
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All results gave a conclusion that STZ-induced DM may induce the impairment of function and expression of Bcrp in brain cortex, and lower levels of insulin may mainly contribute to Bcrp dysfunction in brain.
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27 |
17915193
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Insulin treatment may attenuate the impairment of Bcrp expression and function induced by diabetes.
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28 |
17915193
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All results gave a conclusion that STZ-induced DM may induce the impairment of function and expression of Bcrp in brain cortex, and lower levels of insulin may mainly contribute to Bcrp dysfunction in brain.
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29 |
18374086
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We found that population of human CD133-positive pancreatic cells contains endocrine progenitors expressing neurogenin-3 and cells expressing human telomerase, ABCG2, Oct-3/4, Nanog, and Rex-1, markers of pluripotent stem cells.
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30 |
18622055
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It has also been demonstrated that glyburide is effluxed from the fetal to the maternal circulation by the breast cancer resistance protein (BRCP) and the human multidrug resistance protein 3 (MRP3).
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31 |
19379129
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Moreover, the presence of inductive factors in the Matrigel plus exendin-4 led to an increase in Pdx1 and endocrine genes, such as insulin, islet amyloid polypeptide, glucagon, the glucose transporter GLUT2, chromogranin A and the convertases PC1/3 and PC2 were also detected.
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32 |
19379129
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We identified a population of PaSCs that express the ABCG2+ transporter and have the capacity to transdifferentiate into insulin-producing cells.
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33 |
19937832
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In diabetic rats, Abcb1a, Abcc2, and Abcg2 (apical) were decreased, while Abcc4 (basolateral) was increased.
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34 |
21075088
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The aim of the study was to investigate the influence of diabetes mellitus type 1 on expression and function of the ATP-binding cassette transport proteins P-glycoprotein (Pgp, Abcb1) and breast cancer resistance protein (Bcrp, Abcg2) at the blood-brain barrier and the blood-cerebrospinal fluid barrier formed by the choroid plexus.
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35 |
21075088
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In brain capillary endothelial cells forming the blood-brain barrier, Pgp and Bcrp are located in the luminal membrane while apical/sub-apical localization was described for Pgp in choroid plexus epithelial cells.
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36 |
21075088
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Pgp and Bcrp expression was increased in blood-brain barrier capillaries; in choroid plexus, only Bcrp showed elevated gene expression.
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37 |
21075088
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Consistent with protein expression data, no changes in diabetic animals occurred, suggesting an unaltered function of Pgp and Bcrp.
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38 |
21075088
|
The aim of the study was to investigate the influence of diabetes mellitus type 1 on expression and function of the ATP-binding cassette transport proteins P-glycoprotein (Pgp, Abcb1) and breast cancer resistance protein (Bcrp, Abcg2) at the blood-brain barrier and the blood-cerebrospinal fluid barrier formed by the choroid plexus.
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39 |
21075088
|
In brain capillary endothelial cells forming the blood-brain barrier, Pgp and Bcrp are located in the luminal membrane while apical/sub-apical localization was described for Pgp in choroid plexus epithelial cells.
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40 |
21075088
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Pgp and Bcrp expression was increased in blood-brain barrier capillaries; in choroid plexus, only Bcrp showed elevated gene expression.
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41 |
21075088
|
Consistent with protein expression data, no changes in diabetic animals occurred, suggesting an unaltered function of Pgp and Bcrp.
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42 |
21075088
|
The aim of the study was to investigate the influence of diabetes mellitus type 1 on expression and function of the ATP-binding cassette transport proteins P-glycoprotein (Pgp, Abcb1) and breast cancer resistance protein (Bcrp, Abcg2) at the blood-brain barrier and the blood-cerebrospinal fluid barrier formed by the choroid plexus.
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43 |
21075088
|
In brain capillary endothelial cells forming the blood-brain barrier, Pgp and Bcrp are located in the luminal membrane while apical/sub-apical localization was described for Pgp in choroid plexus epithelial cells.
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44 |
21075088
|
Pgp and Bcrp expression was increased in blood-brain barrier capillaries; in choroid plexus, only Bcrp showed elevated gene expression.
|
45 |
21075088
|
Consistent with protein expression data, no changes in diabetic animals occurred, suggesting an unaltered function of Pgp and Bcrp.
|
46 |
21075088
|
The aim of the study was to investigate the influence of diabetes mellitus type 1 on expression and function of the ATP-binding cassette transport proteins P-glycoprotein (Pgp, Abcb1) and breast cancer resistance protein (Bcrp, Abcg2) at the blood-brain barrier and the blood-cerebrospinal fluid barrier formed by the choroid plexus.
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47 |
21075088
|
In brain capillary endothelial cells forming the blood-brain barrier, Pgp and Bcrp are located in the luminal membrane while apical/sub-apical localization was described for Pgp in choroid plexus epithelial cells.
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48 |
21075088
|
Pgp and Bcrp expression was increased in blood-brain barrier capillaries; in choroid plexus, only Bcrp showed elevated gene expression.
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49 |
21075088
|
Consistent with protein expression data, no changes in diabetic animals occurred, suggesting an unaltered function of Pgp and Bcrp.
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50 |
21118087
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Such transporters include P-glycoprotein (P-gp, gene symbol ABCB1), the breast cancer resistance protein (BCRP, gene symbol ABCG2), and the multidrug resistance proteins (MRPs, gene symbol ABCCs).
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51 |
21602604
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Insulin suppresses the expression and function of breast cancer resistance protein in primary cultures of rat brain microvessel endothelial cells.
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52 |
21602604
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The aim of this study was to investigate the role of insulin in the regulation of breast cancer resistance protein (BCRP) function and expression using primary cultured rat brain microvessel endothelial cells (rBMECs) as an in vitro model of the blood brain barrier (BBB).
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53 |
21602604
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Further results showed that insulin down-regulated the function and expression of BCRP in rBMECs in a concentration-dependent manner.
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54 |
21602604
|
Treatment with an antibody against the insulin receptor abolished the down-regulation of BCRP function and expression that was induced by insulin.
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55 |
21602604
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These results indicate that insulin suppressed the function and expression of BCRPs in rBMEC primary cultures.
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56 |
21602604
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Insulin suppresses the expression and function of breast cancer resistance protein in primary cultures of rat brain microvessel endothelial cells.
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57 |
21602604
|
The aim of this study was to investigate the role of insulin in the regulation of breast cancer resistance protein (BCRP) function and expression using primary cultured rat brain microvessel endothelial cells (rBMECs) as an in vitro model of the blood brain barrier (BBB).
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58 |
21602604
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Further results showed that insulin down-regulated the function and expression of BCRP in rBMECs in a concentration-dependent manner.
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59 |
21602604
|
Treatment with an antibody against the insulin receptor abolished the down-regulation of BCRP function and expression that was induced by insulin.
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60 |
21602604
|
These results indicate that insulin suppressed the function and expression of BCRPs in rBMEC primary cultures.
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61 |
21602604
|
Insulin suppresses the expression and function of breast cancer resistance protein in primary cultures of rat brain microvessel endothelial cells.
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62 |
21602604
|
The aim of this study was to investigate the role of insulin in the regulation of breast cancer resistance protein (BCRP) function and expression using primary cultured rat brain microvessel endothelial cells (rBMECs) as an in vitro model of the blood brain barrier (BBB).
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63 |
21602604
|
Further results showed that insulin down-regulated the function and expression of BCRP in rBMECs in a concentration-dependent manner.
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64 |
21602604
|
Treatment with an antibody against the insulin receptor abolished the down-regulation of BCRP function and expression that was induced by insulin.
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65 |
21602604
|
These results indicate that insulin suppressed the function and expression of BCRPs in rBMEC primary cultures.
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66 |
21602604
|
Insulin suppresses the expression and function of breast cancer resistance protein in primary cultures of rat brain microvessel endothelial cells.
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67 |
21602604
|
The aim of this study was to investigate the role of insulin in the regulation of breast cancer resistance protein (BCRP) function and expression using primary cultured rat brain microvessel endothelial cells (rBMECs) as an in vitro model of the blood brain barrier (BBB).
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68 |
21602604
|
Further results showed that insulin down-regulated the function and expression of BCRP in rBMECs in a concentration-dependent manner.
|
69 |
21602604
|
Treatment with an antibody against the insulin receptor abolished the down-regulation of BCRP function and expression that was induced by insulin.
|
70 |
21602604
|
These results indicate that insulin suppressed the function and expression of BCRPs in rBMEC primary cultures.
|
71 |
21602604
|
Insulin suppresses the expression and function of breast cancer resistance protein in primary cultures of rat brain microvessel endothelial cells.
|
72 |
21602604
|
The aim of this study was to investigate the role of insulin in the regulation of breast cancer resistance protein (BCRP) function and expression using primary cultured rat brain microvessel endothelial cells (rBMECs) as an in vitro model of the blood brain barrier (BBB).
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73 |
21602604
|
Further results showed that insulin down-regulated the function and expression of BCRP in rBMECs in a concentration-dependent manner.
|
74 |
21602604
|
Treatment with an antibody against the insulin receptor abolished the down-regulation of BCRP function and expression that was induced by insulin.
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75 |
21602604
|
These results indicate that insulin suppressed the function and expression of BCRPs in rBMEC primary cultures.
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76 |
22558111
|
To determine if clinically important drug efflux transporter expression is altered in pregnancies complicated by gestational diabetes mellitus (GDM-I) or type 1 diabetes mellitus (T1DM-I), we compared the expression of multidrug resistance protein 1 (MDR1), multidrug resistance-associated protein 2 (MRP2) and the breast cancer resistance protein (BCRP) via western blotting and quantitative real-time polymerase chain reaction in samples obtained from insulin-managed diabetic pregnancies to healthy term-matched controls.
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77 |
22558111
|
Significant changes in the placental protein expression of MDR1, MRP2, and BCRP were not detected (p>0.05).
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78 |
22558111
|
Interestingly, there was a significant, positive correlation observed between plasma hemoglobin A1c levels (a retrospective marker of glycemic control) and both BCRP protein expression (r = 0.45, p<0.05) and BCRP mRNA expression (r = 0.58, p<0.01) in the insulin-managed DM groups.
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79 |
22558111
|
Collectively, the data suggest that the expression of placental efflux transporters is not altered in pregnancies complicated by diabetes when hyperglycemia is managed; however, given the relationship between BCRP expression and plasma hemoglobin A1c levels it is plausible that their expression could change in poorly managed diabetes.
|
80 |
22558111
|
To determine if clinically important drug efflux transporter expression is altered in pregnancies complicated by gestational diabetes mellitus (GDM-I) or type 1 diabetes mellitus (T1DM-I), we compared the expression of multidrug resistance protein 1 (MDR1), multidrug resistance-associated protein 2 (MRP2) and the breast cancer resistance protein (BCRP) via western blotting and quantitative real-time polymerase chain reaction in samples obtained from insulin-managed diabetic pregnancies to healthy term-matched controls.
|
81 |
22558111
|
Significant changes in the placental protein expression of MDR1, MRP2, and BCRP were not detected (p>0.05).
|
82 |
22558111
|
Interestingly, there was a significant, positive correlation observed between plasma hemoglobin A1c levels (a retrospective marker of glycemic control) and both BCRP protein expression (r = 0.45, p<0.05) and BCRP mRNA expression (r = 0.58, p<0.01) in the insulin-managed DM groups.
|
83 |
22558111
|
Collectively, the data suggest that the expression of placental efflux transporters is not altered in pregnancies complicated by diabetes when hyperglycemia is managed; however, given the relationship between BCRP expression and plasma hemoglobin A1c levels it is plausible that their expression could change in poorly managed diabetes.
|
84 |
22558111
|
To determine if clinically important drug efflux transporter expression is altered in pregnancies complicated by gestational diabetes mellitus (GDM-I) or type 1 diabetes mellitus (T1DM-I), we compared the expression of multidrug resistance protein 1 (MDR1), multidrug resistance-associated protein 2 (MRP2) and the breast cancer resistance protein (BCRP) via western blotting and quantitative real-time polymerase chain reaction in samples obtained from insulin-managed diabetic pregnancies to healthy term-matched controls.
|
85 |
22558111
|
Significant changes in the placental protein expression of MDR1, MRP2, and BCRP were not detected (p>0.05).
|
86 |
22558111
|
Interestingly, there was a significant, positive correlation observed between plasma hemoglobin A1c levels (a retrospective marker of glycemic control) and both BCRP protein expression (r = 0.45, p<0.05) and BCRP mRNA expression (r = 0.58, p<0.01) in the insulin-managed DM groups.
|
87 |
22558111
|
Collectively, the data suggest that the expression of placental efflux transporters is not altered in pregnancies complicated by diabetes when hyperglycemia is managed; however, given the relationship between BCRP expression and plasma hemoglobin A1c levels it is plausible that their expression could change in poorly managed diabetes.
|
88 |
22558111
|
To determine if clinically important drug efflux transporter expression is altered in pregnancies complicated by gestational diabetes mellitus (GDM-I) or type 1 diabetes mellitus (T1DM-I), we compared the expression of multidrug resistance protein 1 (MDR1), multidrug resistance-associated protein 2 (MRP2) and the breast cancer resistance protein (BCRP) via western blotting and quantitative real-time polymerase chain reaction in samples obtained from insulin-managed diabetic pregnancies to healthy term-matched controls.
|
89 |
22558111
|
Significant changes in the placental protein expression of MDR1, MRP2, and BCRP were not detected (p>0.05).
|
90 |
22558111
|
Interestingly, there was a significant, positive correlation observed between plasma hemoglobin A1c levels (a retrospective marker of glycemic control) and both BCRP protein expression (r = 0.45, p<0.05) and BCRP mRNA expression (r = 0.58, p<0.01) in the insulin-managed DM groups.
|
91 |
22558111
|
Collectively, the data suggest that the expression of placental efflux transporters is not altered in pregnancies complicated by diabetes when hyperglycemia is managed; however, given the relationship between BCRP expression and plasma hemoglobin A1c levels it is plausible that their expression could change in poorly managed diabetes.
|
92 |
22393122
|
The purpose of this study was to evaluate the contributions of impaired cytochrome P450 and breast cancer resistance protein (BCRP) activity and expression to drug pharmacokinetics under diabetic conditions.
|
93 |
23073734
|
Our results demonstrate that linagliptin is a substrate of organic cation transporter 2 (OCT2) and P-glycoprotein (P-gp) but not of organic anion-transporting polypeptide 1B1 and 1B3; organic anion transporter 1, 3, and 4; OCT1; or organic cation/carnitine transporter 1 and 2, suggesting that OCT2 and P-gp play a role in the disposition of linagliptin in vivo.
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94 |
23073734
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Linagliptin inhibits transcellular transport of digoxin by P-gp with an apparent IC(50) of 66.1 μM, but it did not inhibit activity of multidrug resistance-associated protein 2 and breast cancer resistance protein as represented by transport of probe substrate into membrane vesicles from respective transporter-expressing cells.
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95 |
23073734
|
Linagliptin showed inhibitory potency against only OCT1 and OCT2 out of all major solute carrier transporter isoforms examined, and those inhibition potencies, evaluated using three different in vitro probe substrates, were substrate-specific.
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96 |
23462698
|
Cirrhosis significantly increased ABCC4, 5, ABCG2, and solute carrier organic anion (SLCO) 2B1 mRNA expression and decreased SLCO1B3 mRNA expression in the liver.
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97 |
23462698
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Cirrhosis increased nuclear factor E2-related factor 2 mRNA expression, whereas it decreased pregnane-X-receptor and farnesoid-X-receptor mRNA expression in comparison with normal livers.
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