l-aspartic acid Millipore Search Results


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  • 79
    Millipore l aspartic acid dimethyl ester hydrochloride
    L Aspartic Acid Dimethyl Ester Hydrochloride, supplied by Millipore, used in various techniques. Bioz Stars score: 79/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Millipore l aspartic acid
    L Aspartic Acid, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 192 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Tocris aspartic acid
    Aspartic Acid, supplied by Tocris, used in various techniques. Bioz Stars score: 88/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    77
    Millipore benzyl l aspartic acid
    Benzyl L Aspartic Acid, supplied by Millipore, used in various techniques. Bioz Stars score: 77/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore poly l aspartic acid
    Poly L Aspartic Acid, supplied by Millipore, used in various techniques. Bioz Stars score: 81/100, based on 17 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    86
    Millipore l aspartic acid sodium salt
    L Aspartic Acid Sodium Salt, supplied by Millipore, used in various techniques. Bioz Stars score: 86/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore l aspartic acid sodium salt monohydrate
    L Aspartic Acid Sodium Salt Monohydrate, supplied by Millipore, used in various techniques. Bioz Stars score: 91/100, based on 23 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore l aspartic acid β benzyl ester
    L Aspartic Acid β Benzyl Ester, supplied by Millipore, used in various techniques. Bioz Stars score: 80/100, based on 27 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    78
    Millipore l aspartic acids
    L Aspartic Acids, supplied by Millipore, used in various techniques. Bioz Stars score: 78/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    84
    Millipore l aspartic acid β hydroxamate
    L Aspartic Acid β Hydroxamate, supplied by Millipore, used in various techniques. Bioz Stars score: 84/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore n tert butoxycarbonyl l aspartic acid boc asp oh
    N Tert Butoxycarbonyl L Aspartic Acid Boc Asp Oh, supplied by Millipore, used in various techniques. Bioz Stars score: 77/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore magnesium aspartate
    Magnesium Aspartate, supplied by Millipore, used in various techniques. Bioz Stars score: 75/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore aspartate assay kit
    Aspartate Assay Kit, supplied by Millipore, used in various techniques. Bioz Stars score: 86/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    78
    Millipore anti aspartate igg
    Migration, neuronal differentiation, and synapse formation by E19 immature S1 anlage neurons transplanted to adult S1 cortex undergoing targeted neuronal degeneration. A , Low-magnification image of glutamatergic CPNs in the targeted region of S1 8 weeks after induction of neuronal apoptosis. Arrowheads indicate the region of glutamatergic CPN loss in layer II/III of cortex. B , Camera lucida of a coronal section through an experimental adult mouse brain 6 weeks after transplantation. The inset shows two transplantation sites with transplanted E19-derived neurons double-labeled with PKH 26 and rhodamine fluorescent nanospheres. C , Area boxed in B shows a PKH 26- and nanosphere-labeled E19-derived neuron after migration from the transplantation site ( inset at higher magnification). Transplanted neurons developed large, pyramidal cell bodies typical of adult CPNs. D–G , High-magnification confocal images of E19-derived neurons 12 weeks after transplantation. Arrowheads indicate PKH 26- and nanosphere-labeled E19-derived neurons ( D ) that are immunopositive for NeuN ( E ) and retrogradely labeled with FG from the contralateral S1 cortex ( F ). G , Confocal overlay image of the triple-labeled neurons. Inset shows a triple-labeled neuron ( asterisk ) at higher magnification. Arrows in D–G indicate a NeuN-positive transplanted neuron that is not labeled with FG. H–K , High-magnification confocal images of E19-derived neurons 12 weeks after transplantation. Arrowheads indicate PKH 26- and nanosphere-labeled E19-derived neurons ( H ) that colocalize synaptophysin ( I ) and are retrogradely labeled with FG ( J ). K , A confocal overlay image of triple-labeled neurons. Inset shows a triple-labeled neuron ( asterisk ) at higher magnification. At both 6 and 12 weeks, the injection sites were observed spanning layers II/III through V ( B , L , and O ). L , Injection track showing PKH 26- and nanosphere-labeled E19-derived immature neurons ( red ) 12 weeks after transplantation. M , FG injections to the contralateral cortex 12 weeks after transplantation led to widespread retrograde labeling throughout layer II/III on the transplanted side, distributed well beyond the regions that contained both transplants and endogenous recipient CPNs. N , Negative control immunocytochemistry for aspartate and <t>GABA,</t> omitting the primary antibodies, revealed no cellular labeling. O , Region of experimental cortex at 12 weeks, showing one injection site ( red ), with aspartate-positive endogenous recipient and donor neurons ( green ), and FG retrograde labeling within layer II/III. P–R , E19 donor-derived neurons transplanted to intact control neocortex (injection track indicated by small arrows in P–R ) did not form contralateral projections, although they were located centrally among endogenous recipient CPNs that were retrogradely labeled with FG ( arrowheads in Q and R ). S , Higher magnification of an E19 donor neuron (outlined by arrowheads ; layer V) prelabeled with PKH 26 and nanospheres in intact, control cortex; donor neurons in intact cortex were not retrogradely labeled by FG, but surrounding endogenous recipient CPNs were FG-labeled ( small arrows ). PKH , PKH 26; nano , rhodamine fluorescent nanospheres; syn , synaptophysin; ASP , aspartate. Scale bars: A , 100 μm; C , 20 μm; D : 10 μm (applies to E–K ); L–R , 100 μm; S , 8 μm. Staining procedure for all antibodies: free-floating sections were incubated in primary antibodies for 17–19 hr at 4°C. Labeling was revealed with fluorescent secondary antibodies (1:200 anti-mouse <t>IgG</t> Alexa 488 and 1:250 anti-rabbit IgG Alexa 488), with 2 hr incubation at 4°C. For more details regarding antibody dilutions and sources, see Materials and Methods.
    Anti Aspartate Igg, supplied by Millipore, used in various techniques. Bioz Stars score: 78/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    87
    Millipore α methyl dl aspartic acid
    Migration, neuronal differentiation, and synapse formation by E19 immature S1 anlage neurons transplanted to adult S1 cortex undergoing targeted neuronal degeneration. A , Low-magnification image of glutamatergic CPNs in the targeted region of S1 8 weeks after induction of neuronal apoptosis. Arrowheads indicate the region of glutamatergic CPN loss in layer II/III of cortex. B , Camera lucida of a coronal section through an experimental adult mouse brain 6 weeks after transplantation. The inset shows two transplantation sites with transplanted E19-derived neurons double-labeled with PKH 26 and rhodamine fluorescent nanospheres. C , Area boxed in B shows a PKH 26- and nanosphere-labeled E19-derived neuron after migration from the transplantation site ( inset at higher magnification). Transplanted neurons developed large, pyramidal cell bodies typical of adult CPNs. D–G , High-magnification confocal images of E19-derived neurons 12 weeks after transplantation. Arrowheads indicate PKH 26- and nanosphere-labeled E19-derived neurons ( D ) that are immunopositive for NeuN ( E ) and retrogradely labeled with FG from the contralateral S1 cortex ( F ). G , Confocal overlay image of the triple-labeled neurons. Inset shows a triple-labeled neuron ( asterisk ) at higher magnification. Arrows in D–G indicate a NeuN-positive transplanted neuron that is not labeled with FG. H–K , High-magnification confocal images of E19-derived neurons 12 weeks after transplantation. Arrowheads indicate PKH 26- and nanosphere-labeled E19-derived neurons ( H ) that colocalize synaptophysin ( I ) and are retrogradely labeled with FG ( J ). K , A confocal overlay image of triple-labeled neurons. Inset shows a triple-labeled neuron ( asterisk ) at higher magnification. At both 6 and 12 weeks, the injection sites were observed spanning layers II/III through V ( B , L , and O ). L , Injection track showing PKH 26- and nanosphere-labeled E19-derived immature neurons ( red ) 12 weeks after transplantation. M , FG injections to the contralateral cortex 12 weeks after transplantation led to widespread retrograde labeling throughout layer II/III on the transplanted side, distributed well beyond the regions that contained both transplants and endogenous recipient CPNs. N , Negative control immunocytochemistry for aspartate and <t>GABA,</t> omitting the primary antibodies, revealed no cellular labeling. O , Region of experimental cortex at 12 weeks, showing one injection site ( red ), with aspartate-positive endogenous recipient and donor neurons ( green ), and FG retrograde labeling within layer II/III. P–R , E19 donor-derived neurons transplanted to intact control neocortex (injection track indicated by small arrows in P–R ) did not form contralateral projections, although they were located centrally among endogenous recipient CPNs that were retrogradely labeled with FG ( arrowheads in Q and R ). S , Higher magnification of an E19 donor neuron (outlined by arrowheads ; layer V) prelabeled with PKH 26 and nanospheres in intact, control cortex; donor neurons in intact cortex were not retrogradely labeled by FG, but surrounding endogenous recipient CPNs were FG-labeled ( small arrows ). PKH , PKH 26; nano , rhodamine fluorescent nanospheres; syn , synaptophysin; ASP , aspartate. Scale bars: A , 100 μm; C , 20 μm; D : 10 μm (applies to E–K ); L–R , 100 μm; S , 8 μm. Staining procedure for all antibodies: free-floating sections were incubated in primary antibodies for 17–19 hr at 4°C. Labeling was revealed with fluorescent secondary antibodies (1:200 anti-mouse <t>IgG</t> Alexa 488 and 1:250 anti-rabbit IgG Alexa 488), with 2 hr incubation at 4°C. For more details regarding antibody dilutions and sources, see Materials and Methods.
    α Methyl Dl Aspartic Acid, supplied by Millipore, used in various techniques. Bioz Stars score: 87/100, based on 52 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    77
    Millipore c terminal aspartic acid residue
    Migration, neuronal differentiation, and synapse formation by E19 immature S1 anlage neurons transplanted to adult S1 cortex undergoing targeted neuronal degeneration. A , Low-magnification image of glutamatergic CPNs in the targeted region of S1 8 weeks after induction of neuronal apoptosis. Arrowheads indicate the region of glutamatergic CPN loss in layer II/III of cortex. B , Camera lucida of a coronal section through an experimental adult mouse brain 6 weeks after transplantation. The inset shows two transplantation sites with transplanted E19-derived neurons double-labeled with PKH 26 and rhodamine fluorescent nanospheres. C , Area boxed in B shows a PKH 26- and nanosphere-labeled E19-derived neuron after migration from the transplantation site ( inset at higher magnification). Transplanted neurons developed large, pyramidal cell bodies typical of adult CPNs. D–G , High-magnification confocal images of E19-derived neurons 12 weeks after transplantation. Arrowheads indicate PKH 26- and nanosphere-labeled E19-derived neurons ( D ) that are immunopositive for NeuN ( E ) and retrogradely labeled with FG from the contralateral S1 cortex ( F ). G , Confocal overlay image of the triple-labeled neurons. Inset shows a triple-labeled neuron ( asterisk ) at higher magnification. Arrows in D–G indicate a NeuN-positive transplanted neuron that is not labeled with FG. H–K , High-magnification confocal images of E19-derived neurons 12 weeks after transplantation. Arrowheads indicate PKH 26- and nanosphere-labeled E19-derived neurons ( H ) that colocalize synaptophysin ( I ) and are retrogradely labeled with FG ( J ). K , A confocal overlay image of triple-labeled neurons. Inset shows a triple-labeled neuron ( asterisk ) at higher magnification. At both 6 and 12 weeks, the injection sites were observed spanning layers II/III through V ( B , L , and O ). L , Injection track showing PKH 26- and nanosphere-labeled E19-derived immature neurons ( red ) 12 weeks after transplantation. M , FG injections to the contralateral cortex 12 weeks after transplantation led to widespread retrograde labeling throughout layer II/III on the transplanted side, distributed well beyond the regions that contained both transplants and endogenous recipient CPNs. N , Negative control immunocytochemistry for aspartate and <t>GABA,</t> omitting the primary antibodies, revealed no cellular labeling. O , Region of experimental cortex at 12 weeks, showing one injection site ( red ), with aspartate-positive endogenous recipient and donor neurons ( green ), and FG retrograde labeling within layer II/III. P–R , E19 donor-derived neurons transplanted to intact control neocortex (injection track indicated by small arrows in P–R ) did not form contralateral projections, although they were located centrally among endogenous recipient CPNs that were retrogradely labeled with FG ( arrowheads in Q and R ). S , Higher magnification of an E19 donor neuron (outlined by arrowheads ; layer V) prelabeled with PKH 26 and nanospheres in intact, control cortex; donor neurons in intact cortex were not retrogradely labeled by FG, but surrounding endogenous recipient CPNs were FG-labeled ( small arrows ). PKH , PKH 26; nano , rhodamine fluorescent nanospheres; syn , synaptophysin; ASP , aspartate. Scale bars: A , 100 μm; C , 20 μm; D : 10 μm (applies to E–K ); L–R , 100 μm; S , 8 μm. Staining procedure for all antibodies: free-floating sections were incubated in primary antibodies for 17–19 hr at 4°C. Labeling was revealed with fluorescent secondary antibodies (1:200 anti-mouse <t>IgG</t> Alexa 488 and 1:250 anti-rabbit IgG Alexa 488), with 2 hr incubation at 4°C. For more details regarding antibody dilutions and sources, see Materials and Methods.
    C Terminal Aspartic Acid Residue, supplied by Millipore, used in various techniques. Bioz Stars score: 77/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore cysteinyl aspartate specific proteinase 3
    Migration, neuronal differentiation, and synapse formation by E19 immature S1 anlage neurons transplanted to adult S1 cortex undergoing targeted neuronal degeneration. A , Low-magnification image of glutamatergic CPNs in the targeted region of S1 8 weeks after induction of neuronal apoptosis. Arrowheads indicate the region of glutamatergic CPN loss in layer II/III of cortex. B , Camera lucida of a coronal section through an experimental adult mouse brain 6 weeks after transplantation. The inset shows two transplantation sites with transplanted E19-derived neurons double-labeled with PKH 26 and rhodamine fluorescent nanospheres. C , Area boxed in B shows a PKH 26- and nanosphere-labeled E19-derived neuron after migration from the transplantation site ( inset at higher magnification). Transplanted neurons developed large, pyramidal cell bodies typical of adult CPNs. D–G , High-magnification confocal images of E19-derived neurons 12 weeks after transplantation. Arrowheads indicate PKH 26- and nanosphere-labeled E19-derived neurons ( D ) that are immunopositive for NeuN ( E ) and retrogradely labeled with FG from the contralateral S1 cortex ( F ). G , Confocal overlay image of the triple-labeled neurons. Inset shows a triple-labeled neuron ( asterisk ) at higher magnification. Arrows in D–G indicate a NeuN-positive transplanted neuron that is not labeled with FG. H–K , High-magnification confocal images of E19-derived neurons 12 weeks after transplantation. Arrowheads indicate PKH 26- and nanosphere-labeled E19-derived neurons ( H ) that colocalize synaptophysin ( I ) and are retrogradely labeled with FG ( J ). K , A confocal overlay image of triple-labeled neurons. Inset shows a triple-labeled neuron ( asterisk ) at higher magnification. At both 6 and 12 weeks, the injection sites were observed spanning layers II/III through V ( B , L , and O ). L , Injection track showing PKH 26- and nanosphere-labeled E19-derived immature neurons ( red ) 12 weeks after transplantation. M , FG injections to the contralateral cortex 12 weeks after transplantation led to widespread retrograde labeling throughout layer II/III on the transplanted side, distributed well beyond the regions that contained both transplants and endogenous recipient CPNs. N , Negative control immunocytochemistry for aspartate and <t>GABA,</t> omitting the primary antibodies, revealed no cellular labeling. O , Region of experimental cortex at 12 weeks, showing one injection site ( red ), with aspartate-positive endogenous recipient and donor neurons ( green ), and FG retrograde labeling within layer II/III. P–R , E19 donor-derived neurons transplanted to intact control neocortex (injection track indicated by small arrows in P–R ) did not form contralateral projections, although they were located centrally among endogenous recipient CPNs that were retrogradely labeled with FG ( arrowheads in Q and R ). S , Higher magnification of an E19 donor neuron (outlined by arrowheads ; layer V) prelabeled with PKH 26 and nanospheres in intact, control cortex; donor neurons in intact cortex were not retrogradely labeled by FG, but surrounding endogenous recipient CPNs were FG-labeled ( small arrows ). PKH , PKH 26; nano , rhodamine fluorescent nanospheres; syn , synaptophysin; ASP , aspartate. Scale bars: A , 100 μm; C , 20 μm; D : 10 μm (applies to E–K ); L–R , 100 μm; S , 8 μm. Staining procedure for all antibodies: free-floating sections were incubated in primary antibodies for 17–19 hr at 4°C. Labeling was revealed with fluorescent secondary antibodies (1:200 anti-mouse <t>IgG</t> Alexa 488 and 1:250 anti-rabbit IgG Alexa 488), with 2 hr incubation at 4°C. For more details regarding antibody dilutions and sources, see Materials and Methods.
    Cysteinyl Aspartate Specific Proteinase 3, supplied by Millipore, used in various techniques. Bioz Stars score: 97/100, based on 15 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore arginine glycine aspartic acid rgd peptides
    Migration, neuronal differentiation, and synapse formation by E19 immature S1 anlage neurons transplanted to adult S1 cortex undergoing targeted neuronal degeneration. A , Low-magnification image of glutamatergic CPNs in the targeted region of S1 8 weeks after induction of neuronal apoptosis. Arrowheads indicate the region of glutamatergic CPN loss in layer II/III of cortex. B , Camera lucida of a coronal section through an experimental adult mouse brain 6 weeks after transplantation. The inset shows two transplantation sites with transplanted E19-derived neurons double-labeled with PKH 26 and rhodamine fluorescent nanospheres. C , Area boxed in B shows a PKH 26- and nanosphere-labeled E19-derived neuron after migration from the transplantation site ( inset at higher magnification). Transplanted neurons developed large, pyramidal cell bodies typical of adult CPNs. D–G , High-magnification confocal images of E19-derived neurons 12 weeks after transplantation. Arrowheads indicate PKH 26- and nanosphere-labeled E19-derived neurons ( D ) that are immunopositive for NeuN ( E ) and retrogradely labeled with FG from the contralateral S1 cortex ( F ). G , Confocal overlay image of the triple-labeled neurons. Inset shows a triple-labeled neuron ( asterisk ) at higher magnification. Arrows in D–G indicate a NeuN-positive transplanted neuron that is not labeled with FG. H–K , High-magnification confocal images of E19-derived neurons 12 weeks after transplantation. Arrowheads indicate PKH 26- and nanosphere-labeled E19-derived neurons ( H ) that colocalize synaptophysin ( I ) and are retrogradely labeled with FG ( J ). K , A confocal overlay image of triple-labeled neurons. Inset shows a triple-labeled neuron ( asterisk ) at higher magnification. At both 6 and 12 weeks, the injection sites were observed spanning layers II/III through V ( B , L , and O ). L , Injection track showing PKH 26- and nanosphere-labeled E19-derived immature neurons ( red ) 12 weeks after transplantation. M , FG injections to the contralateral cortex 12 weeks after transplantation led to widespread retrograde labeling throughout layer II/III on the transplanted side, distributed well beyond the regions that contained both transplants and endogenous recipient CPNs. N , Negative control immunocytochemistry for aspartate and <t>GABA,</t> omitting the primary antibodies, revealed no cellular labeling. O , Region of experimental cortex at 12 weeks, showing one injection site ( red ), with aspartate-positive endogenous recipient and donor neurons ( green ), and FG retrograde labeling within layer II/III. P–R , E19 donor-derived neurons transplanted to intact control neocortex (injection track indicated by small arrows in P–R ) did not form contralateral projections, although they were located centrally among endogenous recipient CPNs that were retrogradely labeled with FG ( arrowheads in Q and R ). S , Higher magnification of an E19 donor neuron (outlined by arrowheads ; layer V) prelabeled with PKH 26 and nanospheres in intact, control cortex; donor neurons in intact cortex were not retrogradely labeled by FG, but surrounding endogenous recipient CPNs were FG-labeled ( small arrows ). PKH , PKH 26; nano , rhodamine fluorescent nanospheres; syn , synaptophysin; ASP , aspartate. Scale bars: A , 100 μm; C , 20 μm; D : 10 μm (applies to E–K ); L–R , 100 μm; S , 8 μm. Staining procedure for all antibodies: free-floating sections were incubated in primary antibodies for 17–19 hr at 4°C. Labeling was revealed with fluorescent secondary antibodies (1:200 anti-mouse <t>IgG</t> Alexa 488 and 1:250 anti-rabbit IgG Alexa 488), with 2 hr incubation at 4°C. For more details regarding antibody dilutions and sources, see Materials and Methods.
    Arginine Glycine Aspartic Acid Rgd Peptides, supplied by Millipore, used in various techniques. Bioz Stars score: 78/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore l arginyl l glycyl l aspartic acid
    Migration, neuronal differentiation, and synapse formation by E19 immature S1 anlage neurons transplanted to adult S1 cortex undergoing targeted neuronal degeneration. A , Low-magnification image of glutamatergic CPNs in the targeted region of S1 8 weeks after induction of neuronal apoptosis. Arrowheads indicate the region of glutamatergic CPN loss in layer II/III of cortex. B , Camera lucida of a coronal section through an experimental adult mouse brain 6 weeks after transplantation. The inset shows two transplantation sites with transplanted E19-derived neurons double-labeled with PKH 26 and rhodamine fluorescent nanospheres. C , Area boxed in B shows a PKH 26- and nanosphere-labeled E19-derived neuron after migration from the transplantation site ( inset at higher magnification). Transplanted neurons developed large, pyramidal cell bodies typical of adult CPNs. D–G , High-magnification confocal images of E19-derived neurons 12 weeks after transplantation. Arrowheads indicate PKH 26- and nanosphere-labeled E19-derived neurons ( D ) that are immunopositive for NeuN ( E ) and retrogradely labeled with FG from the contralateral S1 cortex ( F ). G , Confocal overlay image of the triple-labeled neurons. Inset shows a triple-labeled neuron ( asterisk ) at higher magnification. Arrows in D–G indicate a NeuN-positive transplanted neuron that is not labeled with FG. H–K , High-magnification confocal images of E19-derived neurons 12 weeks after transplantation. Arrowheads indicate PKH 26- and nanosphere-labeled E19-derived neurons ( H ) that colocalize synaptophysin ( I ) and are retrogradely labeled with FG ( J ). K , A confocal overlay image of triple-labeled neurons. Inset shows a triple-labeled neuron ( asterisk ) at higher magnification. At both 6 and 12 weeks, the injection sites were observed spanning layers II/III through V ( B , L , and O ). L , Injection track showing PKH 26- and nanosphere-labeled E19-derived immature neurons ( red ) 12 weeks after transplantation. M , FG injections to the contralateral cortex 12 weeks after transplantation led to widespread retrograde labeling throughout layer II/III on the transplanted side, distributed well beyond the regions that contained both transplants and endogenous recipient CPNs. N , Negative control immunocytochemistry for aspartate and <t>GABA,</t> omitting the primary antibodies, revealed no cellular labeling. O , Region of experimental cortex at 12 weeks, showing one injection site ( red ), with aspartate-positive endogenous recipient and donor neurons ( green ), and FG retrograde labeling within layer II/III. P–R , E19 donor-derived neurons transplanted to intact control neocortex (injection track indicated by small arrows in P–R ) did not form contralateral projections, although they were located centrally among endogenous recipient CPNs that were retrogradely labeled with FG ( arrowheads in Q and R ). S , Higher magnification of an E19 donor neuron (outlined by arrowheads ; layer V) prelabeled with PKH 26 and nanospheres in intact, control cortex; donor neurons in intact cortex were not retrogradely labeled by FG, but surrounding endogenous recipient CPNs were FG-labeled ( small arrows ). PKH , PKH 26; nano , rhodamine fluorescent nanospheres; syn , synaptophysin; ASP , aspartate. Scale bars: A , 100 μm; C , 20 μm; D : 10 μm (applies to E–K ); L–R , 100 μm; S , 8 μm. Staining procedure for all antibodies: free-floating sections were incubated in primary antibodies for 17–19 hr at 4°C. Labeling was revealed with fluorescent secondary antibodies (1:200 anti-mouse <t>IgG</t> Alexa 488 and 1:250 anti-rabbit IgG Alexa 488), with 2 hr incubation at 4°C. For more details regarding antibody dilutions and sources, see Materials and Methods.
    L Arginyl L Glycyl L Aspartic Acid, supplied by Millipore, used in various techniques. Bioz Stars score: 76/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Migration, neuronal differentiation, and synapse formation by E19 immature S1 anlage neurons transplanted to adult S1 cortex undergoing targeted neuronal degeneration. A , Low-magnification image of glutamatergic CPNs in the targeted region of S1 8 weeks after induction of neuronal apoptosis. Arrowheads indicate the region of glutamatergic CPN loss in layer II/III of cortex. B , Camera lucida of a coronal section through an experimental adult mouse brain 6 weeks after transplantation. The inset shows two transplantation sites with transplanted E19-derived neurons double-labeled with PKH 26 and rhodamine fluorescent nanospheres. C , Area boxed in B shows a PKH 26- and nanosphere-labeled E19-derived neuron after migration from the transplantation site ( inset at higher magnification). Transplanted neurons developed large, pyramidal cell bodies typical of adult CPNs. D–G , High-magnification confocal images of E19-derived neurons 12 weeks after transplantation. Arrowheads indicate PKH 26- and nanosphere-labeled E19-derived neurons ( D ) that are immunopositive for NeuN ( E ) and retrogradely labeled with FG from the contralateral S1 cortex ( F ). G , Confocal overlay image of the triple-labeled neurons. Inset shows a triple-labeled neuron ( asterisk ) at higher magnification. Arrows in D–G indicate a NeuN-positive transplanted neuron that is not labeled with FG. H–K , High-magnification confocal images of E19-derived neurons 12 weeks after transplantation. Arrowheads indicate PKH 26- and nanosphere-labeled E19-derived neurons ( H ) that colocalize synaptophysin ( I ) and are retrogradely labeled with FG ( J ). K , A confocal overlay image of triple-labeled neurons. Inset shows a triple-labeled neuron ( asterisk ) at higher magnification. At both 6 and 12 weeks, the injection sites were observed spanning layers II/III through V ( B , L , and O ). L , Injection track showing PKH 26- and nanosphere-labeled E19-derived immature neurons ( red ) 12 weeks after transplantation. M , FG injections to the contralateral cortex 12 weeks after transplantation led to widespread retrograde labeling throughout layer II/III on the transplanted side, distributed well beyond the regions that contained both transplants and endogenous recipient CPNs. N , Negative control immunocytochemistry for aspartate and <t>GABA,</t> omitting the primary antibodies, revealed no cellular labeling. O , Region of experimental cortex at 12 weeks, showing one injection site ( red ), with aspartate-positive endogenous recipient and donor neurons ( green ), and FG retrograde labeling within layer II/III. P–R , E19 donor-derived neurons transplanted to intact control neocortex (injection track indicated by small arrows in P–R ) did not form contralateral projections, although they were located centrally among endogenous recipient CPNs that were retrogradely labeled with FG ( arrowheads in Q and R ). S , Higher magnification of an E19 donor neuron (outlined by arrowheads ; layer V) prelabeled with PKH 26 and nanospheres in intact, control cortex; donor neurons in intact cortex were not retrogradely labeled by FG, but surrounding endogenous recipient CPNs were FG-labeled ( small arrows ). PKH , PKH 26; nano , rhodamine fluorescent nanospheres; syn , synaptophysin; ASP , aspartate. Scale bars: A , 100 μm; C , 20 μm; D : 10 μm (applies to E–K ); L–R , 100 μm; S , 8 μm. Staining procedure for all antibodies: free-floating sections were incubated in primary antibodies for 17–19 hr at 4°C. Labeling was revealed with fluorescent secondary antibodies (1:200 anti-mouse <t>IgG</t> Alexa 488 and 1:250 anti-rabbit IgG Alexa 488), with 2 hr incubation at 4°C. For more details regarding antibody dilutions and sources, see Materials and Methods.
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    Migration, neuronal differentiation, and synapse formation by E19 immature S1 anlage neurons transplanted to adult S1 cortex undergoing targeted neuronal degeneration. A , Low-magnification image of glutamatergic CPNs in the targeted region of S1 8 weeks after induction of neuronal apoptosis. Arrowheads indicate the region of glutamatergic CPN loss in layer II/III of cortex. B , Camera lucida of a coronal section through an experimental adult mouse brain 6 weeks after transplantation. The inset shows two transplantation sites with transplanted E19-derived neurons double-labeled with PKH 26 and rhodamine fluorescent nanospheres. C , Area boxed in B shows a PKH 26- and nanosphere-labeled E19-derived neuron after migration from the transplantation site ( inset at higher magnification). Transplanted neurons developed large, pyramidal cell bodies typical of adult CPNs. D–G , High-magnification confocal images of E19-derived neurons 12 weeks after transplantation. Arrowheads indicate PKH 26- and nanosphere-labeled E19-derived neurons ( D ) that are immunopositive for NeuN ( E ) and retrogradely labeled with FG from the contralateral S1 cortex ( F ). G , Confocal overlay image of the triple-labeled neurons. Inset shows a triple-labeled neuron ( asterisk ) at higher magnification. Arrows in D–G indicate a NeuN-positive transplanted neuron that is not labeled with FG. H–K , High-magnification confocal images of E19-derived neurons 12 weeks after transplantation. Arrowheads indicate PKH 26- and nanosphere-labeled E19-derived neurons ( H ) that colocalize synaptophysin ( I ) and are retrogradely labeled with FG ( J ). K , A confocal overlay image of triple-labeled neurons. Inset shows a triple-labeled neuron ( asterisk ) at higher magnification. At both 6 and 12 weeks, the injection sites were observed spanning layers II/III through V ( B , L , and O ). L , Injection track showing PKH 26- and nanosphere-labeled E19-derived immature neurons ( red ) 12 weeks after transplantation. M , FG injections to the contralateral cortex 12 weeks after transplantation led to widespread retrograde labeling throughout layer II/III on the transplanted side, distributed well beyond the regions that contained both transplants and endogenous recipient CPNs. N , Negative control immunocytochemistry for aspartate and <t>GABA,</t> omitting the primary antibodies, revealed no cellular labeling. O , Region of experimental cortex at 12 weeks, showing one injection site ( red ), with aspartate-positive endogenous recipient and donor neurons ( green ), and FG retrograde labeling within layer II/III. P–R , E19 donor-derived neurons transplanted to intact control neocortex (injection track indicated by small arrows in P–R ) did not form contralateral projections, although they were located centrally among endogenous recipient CPNs that were retrogradely labeled with FG ( arrowheads in Q and R ). S , Higher magnification of an E19 donor neuron (outlined by arrowheads ; layer V) prelabeled with PKH 26 and nanospheres in intact, control cortex; donor neurons in intact cortex were not retrogradely labeled by FG, but surrounding endogenous recipient CPNs were FG-labeled ( small arrows ). PKH , PKH 26; nano , rhodamine fluorescent nanospheres; syn , synaptophysin; ASP , aspartate. Scale bars: A , 100 μm; C , 20 μm; D : 10 μm (applies to E–K ); L–R , 100 μm; S , 8 μm. Staining procedure for all antibodies: free-floating sections were incubated in primary antibodies for 17–19 hr at 4°C. Labeling was revealed with fluorescent secondary antibodies (1:200 anti-mouse <t>IgG</t> Alexa 488 and 1:250 anti-rabbit IgG Alexa 488), with 2 hr incubation at 4°C. For more details regarding antibody dilutions and sources, see Materials and Methods.
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    Migration, neuronal differentiation, and synapse formation by E19 immature S1 anlage neurons transplanted to adult S1 cortex undergoing targeted neuronal degeneration. A , Low-magnification image of glutamatergic CPNs in the targeted region of S1 8 weeks after induction of neuronal apoptosis. Arrowheads indicate the region of glutamatergic CPN loss in layer II/III of cortex. B , Camera lucida of a coronal section through an experimental adult mouse brain 6 weeks after transplantation. The inset shows two transplantation sites with transplanted E19-derived neurons double-labeled with PKH 26 and rhodamine fluorescent nanospheres. C , Area boxed in B shows a PKH 26- and nanosphere-labeled E19-derived neuron after migration from the transplantation site ( inset at higher magnification). Transplanted neurons developed large, pyramidal cell bodies typical of adult CPNs. D–G , High-magnification confocal images of E19-derived neurons 12 weeks after transplantation. Arrowheads indicate PKH 26- and nanosphere-labeled E19-derived neurons ( D ) that are immunopositive for NeuN ( E ) and retrogradely labeled with FG from the contralateral S1 cortex ( F ). G , Confocal overlay image of the triple-labeled neurons. Inset shows a triple-labeled neuron ( asterisk ) at higher magnification. Arrows in D–G indicate a NeuN-positive transplanted neuron that is not labeled with FG. H–K , High-magnification confocal images of E19-derived neurons 12 weeks after transplantation. Arrowheads indicate PKH 26- and nanosphere-labeled E19-derived neurons ( H ) that colocalize synaptophysin ( I ) and are retrogradely labeled with FG ( J ). K , A confocal overlay image of triple-labeled neurons. Inset shows a triple-labeled neuron ( asterisk ) at higher magnification. At both 6 and 12 weeks, the injection sites were observed spanning layers II/III through V ( B , L , and O ). L , Injection track showing PKH 26- and nanosphere-labeled E19-derived immature neurons ( red ) 12 weeks after transplantation. M , FG injections to the contralateral cortex 12 weeks after transplantation led to widespread retrograde labeling throughout layer II/III on the transplanted side, distributed well beyond the regions that contained both transplants and endogenous recipient CPNs. N , Negative control immunocytochemistry for aspartate and <t>GABA,</t> omitting the primary antibodies, revealed no cellular labeling. O , Region of experimental cortex at 12 weeks, showing one injection site ( red ), with aspartate-positive endogenous recipient and donor neurons ( green ), and FG retrograde labeling within layer II/III. P–R , E19 donor-derived neurons transplanted to intact control neocortex (injection track indicated by small arrows in P–R ) did not form contralateral projections, although they were located centrally among endogenous recipient CPNs that were retrogradely labeled with FG ( arrowheads in Q and R ). S , Higher magnification of an E19 donor neuron (outlined by arrowheads ; layer V) prelabeled with PKH 26 and nanospheres in intact, control cortex; donor neurons in intact cortex were not retrogradely labeled by FG, but surrounding endogenous recipient CPNs were FG-labeled ( small arrows ). PKH , PKH 26; nano , rhodamine fluorescent nanospheres; syn , synaptophysin; ASP , aspartate. Scale bars: A , 100 μm; C , 20 μm; D : 10 μm (applies to E–K ); L–R , 100 μm; S , 8 μm. Staining procedure for all antibodies: free-floating sections were incubated in primary antibodies for 17–19 hr at 4°C. Labeling was revealed with fluorescent secondary antibodies (1:200 anti-mouse <t>IgG</t> Alexa 488 and 1:250 anti-rabbit IgG Alexa 488), with 2 hr incubation at 4°C. For more details regarding antibody dilutions and sources, see Materials and Methods.
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    Image Search Results


    Migration, neuronal differentiation, and synapse formation by E19 immature S1 anlage neurons transplanted to adult S1 cortex undergoing targeted neuronal degeneration. A , Low-magnification image of glutamatergic CPNs in the targeted region of S1 8 weeks after induction of neuronal apoptosis. Arrowheads indicate the region of glutamatergic CPN loss in layer II/III of cortex. B , Camera lucida of a coronal section through an experimental adult mouse brain 6 weeks after transplantation. The inset shows two transplantation sites with transplanted E19-derived neurons double-labeled with PKH 26 and rhodamine fluorescent nanospheres. C , Area boxed in B shows a PKH 26- and nanosphere-labeled E19-derived neuron after migration from the transplantation site ( inset at higher magnification). Transplanted neurons developed large, pyramidal cell bodies typical of adult CPNs. D–G , High-magnification confocal images of E19-derived neurons 12 weeks after transplantation. Arrowheads indicate PKH 26- and nanosphere-labeled E19-derived neurons ( D ) that are immunopositive for NeuN ( E ) and retrogradely labeled with FG from the contralateral S1 cortex ( F ). G , Confocal overlay image of the triple-labeled neurons. Inset shows a triple-labeled neuron ( asterisk ) at higher magnification. Arrows in D–G indicate a NeuN-positive transplanted neuron that is not labeled with FG. H–K , High-magnification confocal images of E19-derived neurons 12 weeks after transplantation. Arrowheads indicate PKH 26- and nanosphere-labeled E19-derived neurons ( H ) that colocalize synaptophysin ( I ) and are retrogradely labeled with FG ( J ). K , A confocal overlay image of triple-labeled neurons. Inset shows a triple-labeled neuron ( asterisk ) at higher magnification. At both 6 and 12 weeks, the injection sites were observed spanning layers II/III through V ( B , L , and O ). L , Injection track showing PKH 26- and nanosphere-labeled E19-derived immature neurons ( red ) 12 weeks after transplantation. M , FG injections to the contralateral cortex 12 weeks after transplantation led to widespread retrograde labeling throughout layer II/III on the transplanted side, distributed well beyond the regions that contained both transplants and endogenous recipient CPNs. N , Negative control immunocytochemistry for aspartate and GABA, omitting the primary antibodies, revealed no cellular labeling. O , Region of experimental cortex at 12 weeks, showing one injection site ( red ), with aspartate-positive endogenous recipient and donor neurons ( green ), and FG retrograde labeling within layer II/III. P–R , E19 donor-derived neurons transplanted to intact control neocortex (injection track indicated by small arrows in P–R ) did not form contralateral projections, although they were located centrally among endogenous recipient CPNs that were retrogradely labeled with FG ( arrowheads in Q and R ). S , Higher magnification of an E19 donor neuron (outlined by arrowheads ; layer V) prelabeled with PKH 26 and nanospheres in intact, control cortex; donor neurons in intact cortex were not retrogradely labeled by FG, but surrounding endogenous recipient CPNs were FG-labeled ( small arrows ). PKH , PKH 26; nano , rhodamine fluorescent nanospheres; syn , synaptophysin; ASP , aspartate. Scale bars: A , 100 μm; C , 20 μm; D : 10 μm (applies to E–K ); L–R , 100 μm; S , 8 μm. Staining procedure for all antibodies: free-floating sections were incubated in primary antibodies for 17–19 hr at 4°C. Labeling was revealed with fluorescent secondary antibodies (1:200 anti-mouse IgG Alexa 488 and 1:250 anti-rabbit IgG Alexa 488), with 2 hr incubation at 4°C. For more details regarding antibody dilutions and sources, see Materials and Methods.

    Journal: The Journal of Neuroscience

    Article Title: Late-Stage Immature Neocortical Neurons Reconstruct Interhemispheric Connections and Form Synaptic Contacts with Increased Efficiency in Adult Mouse Cortex Undergoing Targeted Neurodegeneration

    doi: 10.1523/JNEUROSCI.22-10-04045.2002

    Figure Lengend Snippet: Migration, neuronal differentiation, and synapse formation by E19 immature S1 anlage neurons transplanted to adult S1 cortex undergoing targeted neuronal degeneration. A , Low-magnification image of glutamatergic CPNs in the targeted region of S1 8 weeks after induction of neuronal apoptosis. Arrowheads indicate the region of glutamatergic CPN loss in layer II/III of cortex. B , Camera lucida of a coronal section through an experimental adult mouse brain 6 weeks after transplantation. The inset shows two transplantation sites with transplanted E19-derived neurons double-labeled with PKH 26 and rhodamine fluorescent nanospheres. C , Area boxed in B shows a PKH 26- and nanosphere-labeled E19-derived neuron after migration from the transplantation site ( inset at higher magnification). Transplanted neurons developed large, pyramidal cell bodies typical of adult CPNs. D–G , High-magnification confocal images of E19-derived neurons 12 weeks after transplantation. Arrowheads indicate PKH 26- and nanosphere-labeled E19-derived neurons ( D ) that are immunopositive for NeuN ( E ) and retrogradely labeled with FG from the contralateral S1 cortex ( F ). G , Confocal overlay image of the triple-labeled neurons. Inset shows a triple-labeled neuron ( asterisk ) at higher magnification. Arrows in D–G indicate a NeuN-positive transplanted neuron that is not labeled with FG. H–K , High-magnification confocal images of E19-derived neurons 12 weeks after transplantation. Arrowheads indicate PKH 26- and nanosphere-labeled E19-derived neurons ( H ) that colocalize synaptophysin ( I ) and are retrogradely labeled with FG ( J ). K , A confocal overlay image of triple-labeled neurons. Inset shows a triple-labeled neuron ( asterisk ) at higher magnification. At both 6 and 12 weeks, the injection sites were observed spanning layers II/III through V ( B , L , and O ). L , Injection track showing PKH 26- and nanosphere-labeled E19-derived immature neurons ( red ) 12 weeks after transplantation. M , FG injections to the contralateral cortex 12 weeks after transplantation led to widespread retrograde labeling throughout layer II/III on the transplanted side, distributed well beyond the regions that contained both transplants and endogenous recipient CPNs. N , Negative control immunocytochemistry for aspartate and GABA, omitting the primary antibodies, revealed no cellular labeling. O , Region of experimental cortex at 12 weeks, showing one injection site ( red ), with aspartate-positive endogenous recipient and donor neurons ( green ), and FG retrograde labeling within layer II/III. P–R , E19 donor-derived neurons transplanted to intact control neocortex (injection track indicated by small arrows in P–R ) did not form contralateral projections, although they were located centrally among endogenous recipient CPNs that were retrogradely labeled with FG ( arrowheads in Q and R ). S , Higher magnification of an E19 donor neuron (outlined by arrowheads ; layer V) prelabeled with PKH 26 and nanospheres in intact, control cortex; donor neurons in intact cortex were not retrogradely labeled by FG, but surrounding endogenous recipient CPNs were FG-labeled ( small arrows ). PKH , PKH 26; nano , rhodamine fluorescent nanospheres; syn , synaptophysin; ASP , aspartate. Scale bars: A , 100 μm; C , 20 μm; D : 10 μm (applies to E–K ); L–R , 100 μm; S , 8 μm. Staining procedure for all antibodies: free-floating sections were incubated in primary antibodies for 17–19 hr at 4°C. Labeling was revealed with fluorescent secondary antibodies (1:200 anti-mouse IgG Alexa 488 and 1:250 anti-rabbit IgG Alexa 488), with 2 hr incubation at 4°C. For more details regarding antibody dilutions and sources, see Materials and Methods.

    Article Snippet: The following primary antibodies were used, at the following dilutions: (1) anti-NeuN IgG (1:100; Chemicon, Temecula, CA; mouse monoclonal); (2) anti-synaptophysin IgG (20 μg/ml; Boehringer Mannheim, Indianapolis, IN; mouse monoclonal); (3) anti-glutamate IgG (1:500; Incstar, Stillwater, MN; mouse monoclonal); (4) anti-aspartate IgG (1:500; Sigma; rabbit polyclonal); (5) anti-GABA IgG (1:500; Incstar; rabbit polyclonal); (6) anti-GABAA receptor β chain IgG1 (10 μg/ml; Boehringer Mannheim; mouse monoclonal); (7) anti-NMDA-R1 IgG2a (1:250; PharMingen, San Diego, CA; mouse monoclonal); (8) anti-glutamate receptor 2/3 IgG (AMPA-R) (1:125; Oncogene Sciences, Uniondale, NY; rabbit polyclonal); and (9) anti-glutamate receptor 5, 6, and 7 IgM (KA-R) (1:250; Pharminogen; mouse monoclonal).

    Techniques: Migration, Transplantation Assay, Derivative Assay, Labeling, Injection, Negative Control, Immunocytochemistry, Staining, Incubation

    Comparison of relative peak positions of GSH and GSH+NAA samples in phosphate buffer saline (PBS) using NMR study over different temperatures. (A) 1D NMR for GSH in PBS solution at 25°C, (B) 1D NMR for GSH+NAA PBS solution at 25°C, (C) GSH+NAA in PBS solution 37°C and, (D) GSH+NAA in PBS solution at 47°C using 500 MHz NMR.

    Journal: Journal of Alzheimer's Disease

    Article Title: A Multi-Center Study on Human Brain Glutathione Conformation using Magnetic Resonance Spectroscopy

    doi: 10.3233/JAD-180648

    Figure Lengend Snippet: Comparison of relative peak positions of GSH and GSH+NAA samples in phosphate buffer saline (PBS) using NMR study over different temperatures. (A) 1D NMR for GSH in PBS solution at 25°C, (B) 1D NMR for GSH+NAA PBS solution at 25°C, (C) GSH+NAA in PBS solution 37°C and, (D) GSH+NAA in PBS solution at 47°C using 500 MHz NMR.

    Article Snippet: Aqueous solutions of GSH (Sigma-Aldrich, USA) and GSH with N-acetyl aspartate (NAA) (Sigma-Aldrich, USA) were prepared in PBS.

    Techniques: Nuclear Magnetic Resonance

    In vivo GSH conformer detection using MEGA-PRESS sequence using 3T Philips and GE scanners with the two MEGA-ON pulse positions, i.e., 4.40 ppm (A) and 4.56 ppm (B) and analysis of relative peak positions and phase of the two GSH conformation using same experimental parameters. Effect of different echo times on the two MEGA-ON pulse positions using both the Philips and GE scanners has been demonstrated for variable TE (120 ms, 125 ms, 130 ms and 140 ms) using MEGA-ON pulse at 4.40 ppm (A) and at 4.56 ppm (B). The selective excitation 180° pulse is applied at 4.40 ppm (for closed conformer) and 4.56 ppm (for extended conformer) (TE = 120 ms and TE = 125 ms give the two out of phase conformer peaks while the same two peaks appear in-phase for TE = 130 ms and TE = 140 ms. Excitation with ON-pulse at 4.40 ppm gives a sharp and heightened peak at ∼2.80 ppm and a broad peak at ∼2.95 ppm; however, ON-pulse at 4.56 ppm results in nearly equal peak shapes and area at two different positions) as the two GSH conformal peaks). The peaks are labeled as: GSH ex refers to Cys-H β extended form; GSH cl refers to Cys-H β closed form; NAA-CH 2 refers to NAA-Aspartate CH 2 group.

    Journal: Journal of Alzheimer's Disease

    Article Title: A Multi-Center Study on Human Brain Glutathione Conformation using Magnetic Resonance Spectroscopy

    doi: 10.3233/JAD-180648

    Figure Lengend Snippet: In vivo GSH conformer detection using MEGA-PRESS sequence using 3T Philips and GE scanners with the two MEGA-ON pulse positions, i.e., 4.40 ppm (A) and 4.56 ppm (B) and analysis of relative peak positions and phase of the two GSH conformation using same experimental parameters. Effect of different echo times on the two MEGA-ON pulse positions using both the Philips and GE scanners has been demonstrated for variable TE (120 ms, 125 ms, 130 ms and 140 ms) using MEGA-ON pulse at 4.40 ppm (A) and at 4.56 ppm (B). The selective excitation 180° pulse is applied at 4.40 ppm (for closed conformer) and 4.56 ppm (for extended conformer) (TE = 120 ms and TE = 125 ms give the two out of phase conformer peaks while the same two peaks appear in-phase for TE = 130 ms and TE = 140 ms. Excitation with ON-pulse at 4.40 ppm gives a sharp and heightened peak at ∼2.80 ppm and a broad peak at ∼2.95 ppm; however, ON-pulse at 4.56 ppm results in nearly equal peak shapes and area at two different positions) as the two GSH conformal peaks). The peaks are labeled as: GSH ex refers to Cys-H β extended form; GSH cl refers to Cys-H β closed form; NAA-CH 2 refers to NAA-Aspartate CH 2 group.

    Article Snippet: Aqueous solutions of GSH (Sigma-Aldrich, USA) and GSH with N-acetyl aspartate (NAA) (Sigma-Aldrich, USA) were prepared in PBS.

    Techniques: In Vivo, Sequencing, Mass Spectrometry, Labeling

    Gut ghrelin increases hepatic glucose production by activating a gut-brain-liver neurocircuitry. a Schematic representation of the working hypothesis. Gut ghrelin was coinfused with tetracaine, which abolishes the ascending neuronal signal to the brain. A subgroup of rats was given MK-801, an NMDA receptor inhibitor, directly into the NTS. In another study, gut ghrelin was infused into rats with HVAG. b Experimental procedure and clamp protocol. Stereotaxic surgeries were conducted on day 1. A duodenal catheter or venous and arterial catheters were implanted on day 7. HVAG was performed immediately before the implantation of the duodenal and vascular catheters. c and d Gut ghrelin infusion decreased GIR and increased HGP. Rats that received tetracaine in the gut, MK-801 in the NTS or HVAG failed to respond to duodenal ghrelin to decrease the GIR and increase HGP. e Suppression of HGP during the clamp expressed as the percentage decrease from basal HGP. f Glucose uptake was unchanged in all groups. NTS, the nucleus of the solitary tract; HVAG, hepatic vagotomy; NMDA, N -methyl- D-aspartate; GIR, glucose infusion rate; HGP, hepatic glucose production. Values are shown as mean ± SEM. * P

    Journal: Cell Communication and Signaling : CCS

    Article Title: Gut ghrelin regulates hepatic glucose production and insulin signaling via a gut-brain-liver pathway

    doi: 10.1186/s12964-019-0321-y

    Figure Lengend Snippet: Gut ghrelin increases hepatic glucose production by activating a gut-brain-liver neurocircuitry. a Schematic representation of the working hypothesis. Gut ghrelin was coinfused with tetracaine, which abolishes the ascending neuronal signal to the brain. A subgroup of rats was given MK-801, an NMDA receptor inhibitor, directly into the NTS. In another study, gut ghrelin was infused into rats with HVAG. b Experimental procedure and clamp protocol. Stereotaxic surgeries were conducted on day 1. A duodenal catheter or venous and arterial catheters were implanted on day 7. HVAG was performed immediately before the implantation of the duodenal and vascular catheters. c and d Gut ghrelin infusion decreased GIR and increased HGP. Rats that received tetracaine in the gut, MK-801 in the NTS or HVAG failed to respond to duodenal ghrelin to decrease the GIR and increase HGP. e Suppression of HGP during the clamp expressed as the percentage decrease from basal HGP. f Glucose uptake was unchanged in all groups. NTS, the nucleus of the solitary tract; HVAG, hepatic vagotomy; NMDA, N -methyl- D-aspartate; GIR, glucose infusion rate; HGP, hepatic glucose production. Values are shown as mean ± SEM. * P

    Article Snippet: In a separate cohort of rats undergoing NTS treatment procedures, MK-801, an N-methyl-D-aspartate (NMDA) receptor inhibitor (0.03 ng/min, Sigma-Aldrich, St Louis, MO, USA), was given at t = 90 to 200 min until the end of the PECs.

    Techniques: