戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (1語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1           Discontinuation vs continuation of cholinesterase inhibitor.
2 and were treated for at least 1 month with a cholinesterase inhibitor.
3 orted by an improvement of these symptoms by cholinesterase inhibitors.
4 detection of organophosphates or exposure to cholinesterase inhibitors.
5 itiated memantine, 1820 (11.2%) discontinued cholinesterase inhibitors.
6 ly accessible both for the substrate and for cholinesterase inhibitors.
7 rase system, and achieve effective dual FAAH/cholinesterase inhibitors.
8 r is as a promising new tool for analysis of cholinesterase inhibitors.
9 in locomotion behavior and responsiveness to cholinesterase inhibitors.
10 onsidered, concentrating upon studies of the cholinesterase inhibitors.
11  was no difference in efficacy among various cholinesterase inhibitors.
12 ntine or when to co-prescribe memantine with cholinesterase inhibitors.
13 1.52), cognitive stimulation combined with a cholinesterase inhibitor (-11.39, -18.38 to -3.93), mass
14 ong 82 patients with DLB and AD treated with cholinesterase inhibitors, 15% (n=12) showed symptomatic
15 f 1806 beneficiaries (2.8%) who discontinued cholinesterase inhibitors (3.4 per 100 person-years) and
16 lzheimer's dementia is commonly treated with cholinesterase inhibitors [4-7]; however, these are mode
17 oman-6-ol (CR-6) with that of the lipophilic cholinesterase inhibitor 6-chlorotacrine results in comp
18 vention patients were more likely to receive cholinesterase inhibitors (79.8% vs 55.1%; P = .002) and
19  organophosphorus compounds (OPs) are potent cholinesterase inhibitors, accounting for their use as i
20            We evaluated the effect of Acetyl-cholinesterase-inhibitors (AChEIs) on cognitive decline
21      We show that a brief treatment with the cholinesterase inhibitor aldicarb induces a form of pres
22  a systematic screening of the effect of the cholinesterase inhibitor aldicarb on the rate of pharyng
23             Pharmacological assays using the cholinesterase inhibitor aldicarb suggest that VAs and G
24  have an exaggerated paralytic response to a cholinesterase inhibitor, aldicarb.
25 chotic drugs alone (1.33, 1.24 to 1.43), and cholinesterase inhibitors alone (1.17, 1.10 to 1.24).
26 ures for different treatment periods: use of cholinesterase inhibitors alone, antipsychotic drugs alo
27 chotic drugs, antipsychotic drugs alone, and cholinesterase inhibitors alone, respectively.
28 tter addressed by multifunctional drugs than cholinesterase inhibitors alone.
29            Physostigmine (a centrally active cholinesterase inhibitor) also dose-dependently inhibite
30 d to determine the effects of galantamine, a cholinesterase inhibitor and a nicotinic allosteric pote
31 cluding a phenserine analogue as a potential cholinesterase inhibitor and constrained tryptamine deri
32 y measured the effects of treatment with the cholinesterase inhibitor and nicotinic receptor modulato
33 mal limb muscles, response to treatment with cholinesterase inhibitors and 3,4-diaminopyridine, and t
34 er of direct acting muscarinic agonists, two cholinesterase inhibitors and a putative m1 agonist/musc
35 ollowed by treatment with the combination of cholinesterase inhibitors and antipsychotic drugs (1.35,
36 1 (8.98 to 9.86) for use of a combination of cholinesterase inhibitors and antipsychotic drugs, antip
37 ipsychotic drugs alone, and a combination of cholinesterase inhibitors and antipsychotic drugs, compa
38 n the risk of falls and fractures and use of cholinesterase inhibitors and antipsychotic drugs.
39 studies demonstrated available drugs such as cholinesterase inhibitors and ChAT inducers increased th
40                                              Cholinesterase inhibitors and corticosteroids have been
41                                              Cholinesterase inhibitors and memantine do not have regu
42 for randomised, placebo-controlled trials on cholinesterase inhibitors and memantine in patients with
43 sess the evidence for efficacy and safety of cholinesterase inhibitors and memantine in vascular deme
44                                              Cholinesterase inhibitors and memantine may benefit pers
45                                              Cholinesterase inhibitors and memantine produce small be
46                                              Cholinesterase inhibitors and memantine slightly reduced
47           Cognitive enhancing drugs, such as cholinesterase inhibitors and methylphenidate, are used
48 ortant implications for the long-term use of cholinesterase inhibitors and other cholinomimetics in t
49           Evidence regarding the benefits of cholinesterase inhibitors and other therapeutic options
50 ning the interaction between carbamate-based cholinesterase inhibitors and their enzyme target.
51 r exploration such as escitalopram, lithium, cholinesterase inhibitors and vitamin D.
52  preservation of the cholinergic system (via cholinesterase inhibitors) and hippocampal neurons (via
53 erapy, cognitive stimulation combined with a cholinesterase inhibitor, and cognitive stimulation comb
54                              Antipsychotics, cholinesterase inhibitors, and alpha-2 agonists are the
55                  Short-term treatment with a cholinesterase inhibitor appears to enhance the activity
56 cotinic cholinergic agonists are used, or if cholinesterase inhibitors are combined with other agents
57                                              Cholinesterase inhibitors are commonly used to improve c
58 results from randomized controlled trials of cholinesterase inhibitors are conflicting.
59               More effective treatments than cholinesterase inhibitors are needed for Alzheimer's dis
60 erate clinically detected Alzheimer disease, cholinesterase inhibitors are somewhat effective in slow
61                                              Cholinesterase inhibitors are the primary treatment for
62                                        While cholinesterase inhibitors are used as drug treatments fo
63 , and fewer than 20% of patients stop taking cholinesterase inhibitors because of side effects.
64 , diarrhoea, and insomnia) occurred with the cholinesterase inhibitors, but not with memantine.
65 ifos and diazinon are bioactivated to potent cholinesterase inhibitors by cytochrome P-450 systems.
66 results indicate that one mechanism by which cholinesterase inhibitors can improve memory is by enhan
67             Phenserine, a recently developed cholinesterase inhibitor (ChEI), has been reported to re
68                                              Cholinesterase inhibitors (ChEIs) are specific Alzheimer
69                                              Cholinesterase inhibitors (ChEIs) may be effective treat
70 nd visual) were also affected in MCI and (2) cholinesterase inhibitors (ChEIs), one of the therapies
71                          Therefore, use of a cholinesterase inhibitor (ChI) might improve cognitive f
72                  Administration of a central cholinesterase inhibitor (ChI) partially restored the su
73                                              Cholinesterase inhibitor (ChI) therapy for mixed dementi
74                      Prescription records of cholinesterase inhibitors confirmed the diagnosis of maj
75                         In persons with MCI, cholinesterase inhibitors did not reduce dementia risk (
76 while neostigmine (a peripherally restricted cholinesterase inhibitor) did not.
77 he brains of healthy human subjects with the cholinesterase inhibitor donepezil (trade name: Aricept)
78 zed by fusing the pharmacophoric features of cholinesterase inhibitor donepezil and diarylthiazole as
79  found that cholinergic enhancement with the cholinesterase inhibitor donepezil improved target detec
80                                          The cholinesterase inhibitor donepezil was administered to n
81                                          The cholinesterase inhibitor, donepezil (Aricept), reverses
82                                              Cholinesterase inhibitor drugs improve cognition and neu
83 ch might help explain the limited success of cholinesterase inhibitor drugs in treating memory impair
84                               In contrast, a cholinesterase inhibitor, eserine, although significantl
85                                Stable use of cholinesterase inhibitors, estrogen, low-dose aspirin, a
86 um samples from individuals asymptomatic for cholinesterase inhibitor exposure were analyzed using th
87 euptake inhibitors for psychiatric symptoms, cholinesterase inhibitors for cognition).
88   Clinical trials have shown the benefits of cholinesterase inhibitors for the treatment of mild-to-m
89 magnetic scavenging technique for extracting cholinesterase inhibitors from aqueous matrixes using bi
90 r a psychopharmacological challenge with the cholinesterase inhibitor galantamine (Reminyl).
91  trials of memantine in patients receiving a cholinesterase inhibitor have been performed.
92                  These results indicate that cholinesterase inhibitors have a modest beneficial impac
93  PSP, but trials of cholinergic agonists and cholinesterase inhibitors have failed to show improvemen
94      The combination of the scaffolds of the cholinesterase inhibitor huprine Y and the antioxidant c
95 reatment typically includes symptomatic oral cholinesterase inhibitors, immunosuppression, and immuno
96                                              Cholinesterase inhibitors improve attention, as well as
97                                              Cholinesterase inhibitors improve cognitive outcomes in
98 ompared with placebo, patients randomized to cholinesterase inhibitors improved 0.1 SDs on ADL scales
99 ompared with placebo, patients randomized to cholinesterase inhibitors improved 1.72 points on the NP
100 treatment effects associated with the use of cholinesterase inhibitors in these populations.
101 cal symptomatic cholinergic therapy based on cholinesterase inhibitors is judiciously discussed for i
102                               Treatment with cholinesterase inhibitors is well tolerated by most pati
103 dults with moderate to severe CATD receiving cholinesterase inhibitors, low- to insufficient-strength
104 ver, a combination of an M2 antagonist and a cholinesterase inhibitor may reach the maximal disease-m
105 h cognitive and behavioral disturbances, and cholinesterase inhibitors may improve behavior in Alzhei
106     Our findings suggest that treatment with cholinesterase inhibitors may improve muscle function in
107                                              Cholinesterase inhibitors may improve symptoms of dement
108        Alzheimer disease can be treated with cholinesterase inhibitors, memantine, and antiamyloid im
109                                          The cholinesterase inhibitor methyl paraoxon significantly d
110           Six to 12 months of treatment with cholinesterase inhibitors modestly slows the decline of
111 olinergic stimulation with pyridostigmine, a cholinesterase inhibitor, modulates heart and spleen imm
112                      Known adverse events of cholinesterase inhibitors (nausea, vomiting, anorexia) w
113  with NAC in combination with the peripheral cholinesterase inhibitor neostigmine showed prolonged su
114                       In the presence of the cholinesterase inhibitor neostigmine, EFS led to an addi
115 ceptor (mAChR) agonist, oxotremorine, or the cholinesterase inhibitor, neostigmine (NEOS), in the rRP
116 ny patients' preference to take memantine or cholinesterase inhibitors off-label rather than particip
117 te administration of rivastigmine, a central cholinesterase inhibitor, on patterns of brain activatio
118 Central Register and/or by prescription of a cholinesterase inhibitor or memantine hydrochloride from
119 cision to initiate a trial of therapy with a cholinesterase inhibitor or memantine on individualized
120                   Concomitant treatment with cholinesterase inhibitors or memantine was permitted.
121                                The effect of cholinesterase inhibitors or other treatments on persons
122  from our laboratory have shown that a novel cholinesterase inhibitor, phenserine, reduces betaAPP le
123   However, the administration of neither the cholinesterase inhibitor physostigmine nor the benzodiaz
124                 We studied the effect of the cholinesterase inhibitor physostigmine on subcomponents
125 ned ACh elevation through application of the cholinesterase inhibitor physostigmine suppressed glutam
126 ith age, and attenuation by the nonselective cholinesterase inhibitor physostigmine, but no attenuati
127 artially susceptible to improvement with the cholinesterase inhibitor physostigmine.
128                                              Cholinesterase inhibitors positively affect cognition in
129                                              Cholinesterase inhibitors produce small improvements in
130 dence suggested that, compared with placebo, cholinesterase inhibitors produced small average improve
131 rior administration of muscarinic agonist or cholinesterase inhibitor) produced robust but transient
132 ncement of cholinergic neurotransmission via cholinesterase inhibitors represents the main available
133                                 Donepezil, a cholinesterase inhibitor, restored performance in animal
134                                          The cholinesterase inhibitors rivastigmine, donepezil, and m
135                                    Whether a cholinesterase inhibitor should be used as augmentation
136 rophosphate (DCP), a model organophosphorous cholinesterase inhibitor simulant.
137 ly reduced short-term cognitive decline, and cholinesterase inhibitors slightly reduced reported func
138                                          The cholinesterase inhibitors, tacrine and physostigmine, an
139                                 Unlike other cholinesterase inhibitors tested, rivastigmine inhibited
140 t dimethoxybenzilidene anabaseine (DMXB) and cholinesterase inhibitor tetrahydroaminoacridine (THA) w
141                   We tested the premise that cholinesterase inhibitor therapy should target butyrylch
142 vides evidence for the long-term efficacy of cholinesterase inhibitor therapy suggesting a disease-mo
143 ia responds poorly to nonpharmacological and cholinesterase inhibitor therapy, and although corticost
144 of 91 participants, all receiving background cholinesterase inhibitor therapy, were randomized 1:1 be
145                                   The use of cholinesterase inhibitors to correct the cholinergic def
146 ddition, we need to know when to switch from cholinesterase inhibitors to memantine or when to co-pre
147 ehavioural symptoms, which is often added to cholinesterase inhibitors to potentiate their effect and
148 in injection, we administered neostigmine, a cholinesterase inhibitor, to artificially raise ACh.
149 es that provided a diagnosis, treatment with cholinesterase inhibitor together with physical and occu
150 blocking drugs and encapsulates them, making cholinesterase inhibitors unnecessary.
151                 In this study, discontinuing cholinesterase inhibitors upon memantine initiation was
152                               Galantamine, a cholinesterase inhibitor used in Alzheimer's disease, si
153 f major neurocognitive disorders; all use of cholinesterase inhibitors was reviewed by experts.
154                              Rivastigmine, a cholinesterase inhibitor, was tested in a group of clini
155  effects of metrifonate, a second generation cholinesterase inhibitor, were examined on CA1 pyramidal
156                                Discontinuing cholinesterase inhibitors when initiating memantine in p
157 -inflammatory therapy, immune-modulators and cholinesterase inhibitors which could lead to new therap
158 ucted to assess the impact of galantamine, a cholinesterase inhibitor with nicotinic-receptor-modulat

 
Page Top