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1                                              AADC deficient patients fail to produce normal levels of
2                                              AADC immunopositive (AADC +) cells were also counted in
3                                              AADC levels did not decrease during development, and adu
4                                              AADC secreted much higher levels of IL-10, but lower lev
5      Results: Thirty-five studies (29 DAT, 6 AADC, no vesicular monoamine type 2 studies) with 356 MS
6 lates key disease features, including absent AADC enzyme activity and dysregulated dopamine metabolis
7 e conclude that even minute levels of active AADC are sufficient to allow for substantial amounts of
8 ity response to L-DOPA in the presence of an AADC inhibitor showed a delayed onset, yet greater inten
9 I taste bud cells (NTPdase 2, PLC-beta2, and AADC, respectively).
10 n rats and humans, co-expression of INMT and AADC mRNA in rat brain and periphery, and brain concentr
11 ation approaches, we demonstrate that TH and AADC associate with VMAT(2)-containing synaptic vesicles
12                       In rat striata, TH and AADC co-immunoprecipitate with VMAT(2), whereas in PC 12
13 T(2) involved in the interaction with TH and AADC.
14 s using 6-[(18)F]fluorodopa (FDOPA) (another AADC substrate) to measure how striatal PET signal and a
15 atal form of infantile Parkinsonism known as AADC deficiency.
16 t biomarker evidence of restoration of brain AADC activity.
17  LAT1 transport but is not decarboxylated by AADC.
18 be mediated by 5-HT1B receptors expressed by AADC cells.
19                    The production of 5-HT by AADC cells, together with an upregulation of 5-HT2 recep
20 trophysiology, we show that 5-HT produced by AADC cells increases the excitability of spinal motoneur
21                  A single infusion of BALB/c AADC to quiescent B10 recipients induced alloantigen-spe
22 , relies in part on DOPA decarboxylase (DDC, AADC), an enzyme that is required for normative neural o
23 lasms that possess amino acid decarboxylase (AADC) activity and can theoretically be imaged by (18)F-
24 ized by aromatic-L-amino acid decarboxylase (AADC) and indolethylamine-N-methyltransferase (INMT).
25 ed with aromatic L-amino acid decarboxylase (AADC) and VMAT-2 genes.
26  enzyme aromatic-L-amino acid decarboxylase (AADC) and, when incubated with the dopamine precursor, 3
27 (TPH) and aromatic amino acid decarboxylase (AADC) are expressed in taste cells.
28     The aromatic L-amino-acid decarboxylase (AADC) defect appears to be consistently smaller than the
29         Aromatic l-amino acid decarboxylase (AADC) deficiency is a complex inherited neurological dis
30         Aromatic L-amino acid decarboxylase (AADC) deficiency is a rare genetic disorder characterize
31         Aromatic l-amino acid decarboxylase (AADC) deficiency is an inborn error of monoamine neurotr
32         Aromatic l-amino acid decarboxylase (AADC) deficiency is an inherited disease that causes dep
33 en with aromatic l-amino acid decarboxylase (AADC) deficiency suffer from severe motor dysfunction.
34  in the L-aromatic amino acid decarboxylase (AADC) enzyme was replicated in a meta-analysis of 3 inde
35  enzyme Aromatic L-amino acid decarboxylase (AADC) for its production.
36 The rat aromatic l-amino acid decarboxylase (AADC) gene contains alternative promoters which direct e
37  in the aromatic l-amino acid decarboxylase (AADC) gene result in a severe depletion of its namesake
38 TH) and L-aromatic amino acid decarboxylase (AADC) in animals housed under long photoperiod (LD) or S
39 vity of aromatic l-amino acid decarboxylase (AADC) in the corpus striatum (CS) and substantia nigra (
40 ctions of aromatic amino acid decarboxylase (AADC) in the proximal tubule, previous studies have not
41 on of the aromatic amino acid decarboxylase (AADC) inhibitor m-hydroxybenzylhydrazine attenuated thes
42  enzyme aromatic l-amino acid decarboxylase (AADC) occur not only near the central canal, as reported
43  enzyme aromatic l-amino acid decarboxylase (AADC) or the TH cofactor tetrahydrobiopterin (BH4) could
44           Aromatic amino acid decarboxylase (AADC) then converts di-OH-phenylalanine into DA.
45 lation by aromatic amino acid decarboxylase (AADC), an enzyme overexpressed in these malignancies.
46 e (TH), aromatic l-amino acid decarboxylase (AADC), and GTP cyclohydrolase I (GCH1) transcription; in
47 er (DAT), aromatic amino acid decarboxylase (AADC), or vesicular monoamine type 2 were investigated.
48 ates of aromatic l-amino acid decarboxylase (AADC), the level of which is enhanced in endocrine tumor
49  enzyme aromatic L-amino acid decarboxylase (AADC), which synthesizes trace amines directly from diet
50 he enzyme aromatic amino acid decarboxylase (AADC).
51 g enzyme, aromatic amino acid decarboxylase (AADC).
52 TH), aromatic amino acid dopa decarboxylase (AADC), and GTP cyclohydrolase 1 (CH1) in a single transc
53 rmation pathway (acetoacetate decarboxylase [AADC] and coenzyme A-transferase [CoAT]) of Clostridium
54 isease, aromatic l-amino acid decarboxylase [AADC] deficiency, and giant axonal neuropathy), ocular d
55 C; also known as L-amino acid decarboxylase; AADC) is involved in the synthesis of dopamine, norepine
56 erized aromatic l-amino acid decarboxylases (AADCs) and aromatic aldehyde synthases (AASs), which pla
57        Aromatic L-amino acid decarboxylases (AADCs) are key enzymes operating at the interface betwee
58 0, encoding pyridoxal 5'-phosphate-dependent AADCs with high homology to the recently identified Petu
59  mg/kg) and phencyclidine (4 mg/kg) elevated AADC activity in both the CS and SN (2- to 3-fold).
60 d Nicotiana benthamiana showed that all five AADC/AAS genes identified in the P trichocarpa genome en
61 tic neurons were strongly immunoreactive for AADC.
62            There is no optimal treatment for AADC deficiency and few truly good models in which to in
63 tants represent a novel, mild model of human AADC deficiency.
64 ated virus (AAV) vector containing the human AADC gene (AAV2-hAADC) in four children with AADC defici
65                         AADC immunopositive (AADC +) cells were also counted in the median eminence.
66                     The phenotypic change in AADC cells appears to result from a loss of inhibition b
67                              This decline in AADC+ cells may play a role in SD-induced changes in hyp
68            Similarly pronounced increases in AADC activity in CS (1.9-fold) and SN (2.8-fold) were de
69              Even more striking increases in AADC were noted with 40 mg/kg amantadine (3.8-fold for C
70 g alpha2-adrenoceptors, profoundly increases AADC activity, more especially in the SN than CS.
71 nificant because of limited data, aromatic l-AADC results paralleled the DAT findings.
72 nzyme L-aromatic amino acid decarboxylase (L-AADC) in neural and nonneural tissue, on blood pressure
73 dministration of carbidopa, which inhibits L-AADC outside the blood-brain barrier, blunted both the i
74 nsection of the rat spinal cord at S2 level, AADC cells distal to the lesion acquire the ability to p
75 we generated mice with selective deletion of AADC in the kidney proximal tubules (referred to herein
76    Despite the significant downregulation of AADC in these strains, there were no concomitant effects
77 cally reduces the conformational dynamics of AADC, potentially lowering its binding capacity to a cof
78 which do not express the nonneuronal form of AADC by transient transfection.
79 ecific expression of the nonneuronal form of AADC mRNA is HNF-1.
80 which do not express the nonneuronal form of AADC resulted in activation of transfected AADC nonneuro
81 re inhibited by benserazide, an inhibitor of AADC.
82 that all three strains exhibit low levels of AADC compared to the plasmid control [ATCC 824(pSOS95del
83  In contrast, FMT remains a purer measure of AADC function.
84                         In vivo migration of AADC to secondary lymphoid tissue was not impaired.
85 ived midbrain dopaminergic neuronal model of AADC deficiency from induced pluripotent stem cells.
86                                The number of AADC + cells was also reduced in the median eminence of
87 duced a significant decline in the number of AADC + cells.
88      Inhibition of monoamine receptors or of AADC, or even an increase in inhaled oxygen, produces su
89 ce insight into the regulatory properties of AADC and demonstrate their therapeutic potential in vasc
90 ight into the neurodevelopmental sequelae of AADC deficiency, as well as a robust platform to investi
91 efinitive diagnosis and clinical symptoms of AADC deficiency (hypotonia, dystonia, and oculogyric cri
92 porter 2 defects, suggesting upregulation of AADC function in PD.
93 tion reduces the maximum kinetic velocity of AADC, hence lowering 5-HT levels.
94 or muscarinic receptors is without effect on AADC in either brain region.
95 ect the number of TH immunopositive (TH+) or AADC + cells in the caudal periventricular nuclei.
96                         A survey of putative AADC/AAS gene pairs in the genomes of other plants sugge
97 A 966 (5 mg/kg, not 1 mg/kg) modestly raised AADC activity in CS (0.45-fold) and not SN.
98 ssion of the nonneuronal promoter of the rat AADC gene in the kidney epithelial cell line LLC-PK1 and
99 atic and biochemical analyses on recombinant AADC predicted that the activity of one variant could be
100 dicate that this phenotypic change in spinal AADC cells is initiated by the loss of descending 5-HT p
101 tal neurons transduced with this vector, TH, AADC, and CH1 proteins can all be detected.
102 ence of fragments involved in the VMAT(2)/TH/AADC interaction.
103                 These findings indicate that AADC cells are a potential source of 5-HT at spinal leve
104                  These findings suggest that AADC does not limit acetone formation and, thus, we targ
105                                          The AADC-expanded allogeneic CD4+CD25+ T cells showed enhanc
106 ly by CTLA4-Ig, administered 1 day after the AADC.
107 roduce asRNAs of various lengths against the AADC (adc) transcript.
108 roaches, we identified a polymorphism in the AADC enzyme that contributes to somatic symptoms through
109 ss a stable but minimally active form of the AADC protein.
110 8)F-FDOPA PET results, pretreatment with the AADC inhibitor S-carbidopa did not affect the (18)F-l-FE
111 , the three different asRNAs directed toward AADC, along with previously reported clostridial asRNAs,
112 f AADC resulted in activation of transfected AADC nonneuronal promoter constructs.
113  tyrosine to DOPA and subsequently to DA via AADC.
114 fted with either control cells or cells with AADC alone.
115 AADC gene (AAV2-hAADC) in four children with AADC deficiency (aged 4-6 years).
116      Midbrain gene delivery in children with AADC deficiency is feasible and safe, and leads to clini
117 t improve motor development in children with AADC deficiency.
118      Notably, INMT mRNA was colocalized with AADC transcript in rat brain tissues, in contrast to rat
119 ent) and a movement disorder compatible with AADC deficiency (one patient).
120 of (18)F-FDOPA significantly correlated with AADC expression (n = 15 nonhepatic tumors; maximum stand
121 -FDOPA PET were measured and correlated with AADC messenger RNA level in tumor tissue.
122                          By correlating with AADC expression, (18)F-FDOPA PET might serve as a useful
123 d little overlapping expression of INMT with AADC transcripts.
124 probably independent of any interaction with AADC.
125 n dopamine and serotonin levels of mice with AADC deficiency.
126 is highly prevalent in Chinese patients with AADC deficiency.

 
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