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1 al therapy, the most promising of which is D-cycloserine.
2 s including beta-lactams, polymyxin B, and d-cycloserine.
3 he algD operon undergoes high induction by D-cycloserine.
4 a complete lack of PalgD-cat induction by D-cycloserine.
5 echanism of alanine racemase inactivation by cycloserine.
6 dex increased 100% in the presence of 2 mm l-cycloserine.
7 tuberculosis fails to become resistant to D-cycloserine.
8 mptoms worsen, as previously reported with D-cycloserine.
9 ontrolled trial of 50 mg and 100 mg/day of D-cycloserine.
10 anidine and enrichment with penicillin and D-cycloserine.
11 ith response of negative symptoms to 50-mg D-cycloserine.
12 ularly for toxic second-line drugs such as D-cycloserine.
13 cine(B) site on the NMDA receptor, such as d-cycloserine.
14 in comparison with the enzyme inactivated by cycloserine.
15 ion of the NMDA receptor partial coagonist d-cycloserine.
16 1 to either iTBS plus placebo or iTBS plus D-cycloserine (100 mg) for the first 2 weeks followed by i
18 e mean reduction in negative symptoms with D-cycloserine (23%) was significantly greater than with pl
20 microg/ml; clarithromycin, 1.25 microg/ml; D-cycloserine, 25 microg/ml; ethambutol, 20 microg/ml; and
22 received linezolid, with a subset receiving cycloserine (5), clofazimine (5), delamanid (4), and bed
23 rtual reality exposure were augmented with D-cycloserine (50 mg) or alprazolam (0.25 mg) in a double-
24 ia for deficit syndrome were randomized to D-cycloserine, 50 mg/d (n=23) or placebo (n=24) added to t
32 lfactory threat extinction in aged rats by D-cycloserine, a partial NMDAR agonist, suggests that the
35 ted that the NMDA receptor partial agonist d-cycloserine administered after pavlovian extinction of c
37 osure therapy for SAD may be enhanced with d-cycloserine, an agonist at the glutamatergic N-methyl-d-
39 -propanol and, to a much lesser extent, by L-cycloserine, an inhibitor of de novo ceramide synthesis.
43 ith an average of 5.3+/-1.3 drugs, including cycloserine, an injectable drug, and a fluoroquinolone.
46 de, para-aminosalicylic acid, linezolid, and cycloserine and compared with Bactec MGIT results for py
47 e adduct is similar to that formed between d-cycloserine and d-a-AT or alanine racemase (Ala-Rac) in
48 o inhibitors of sphingolipid biosynthesis, L-cycloserine and fumonisin B1, prevented the observed acc
49 ted the assay by performing it to identify D-Cycloserine and furan-based benzene-derived compounds wi
51 mbined with data from previous trials with D-cycloserine and glycine, suggest that agonists at the gl
54 differences between glycine and placebo or D-cycloserine and placebo subjects on the average cognitio
56 pressant efficacy of ketamine, and perhaps D-cycloserine and rapastinel, holds promise for future glu
57 rtial agonists at the NMDA coagonist site, d-cycloserine and rapastinel, significantly reduced depres
59 inhibitors of de novo ceramide synthesis (l-cycloserine) and CerS (fumonisin B(1)) in cell viability
60 ncomycin, ristocetin), peptides (bacitracin, cycloserine), and chloramphenicol were found to differ s
61 e synthesis, fumonisin B(1), myriocin, and l-cycloserine, and 4-HPR transiently activated serine palm
65 ctamase in M. xanthus, such as ampicillin, D-cycloserine, and phosphomycin, accelerates the onset of
66 d loss of function conferred resistance to D-cycloserine, and susceptibility to the drug was partiall
70 upport for the use of short-term dosing of d-cycloserine as an adjunctive intervention to exposure th
71 These data provide support for the use of D-cycloserine as an augmentation of behavior therapy for O
72 nking, and support testing of D-serine and D-cycloserine as immediately accessible, FDA-approved drug
81 0 min, followed by inoculation onto modified cycloserine cefoxitin fructose agar with and without hor
82 for 10 min before inoculation onto modified cycloserine, cefoxitin, and fructose agar with horse blo
84 horse blood and taurocholate (CCFA-HT), and cycloserine-cefoxitin mannitol broth with taurocholate a
85 have developed a reduced-cost substitute for cycloserine-cefoxitin-fructose agar (CCFA), which is an
87 dvanced Clinical Diagnostics) and culture on cycloserine-cefoxitin-fructose agar followed by determin
88 iated disease were prospectively cultured on cycloserine-cefoxitin-fructose agar following alcohol sh
92 e precursors isolated after treatment with d-cycloserine consisted entirely of N-glycolyl muropeptide
93 isolated from M. tuberculosis treated with d-cycloserine contained only N-glycolylmuramyl-tripeptide
95 , and levofloxacin (Lfx) and reinforced with cycloserine (Cs) and clofazimine (Cfz), delamanid (Dlm)
96 glutamic acid, aspartyl-histidine (Asp-His), cycloserine (cSer), and arginine, which provided a stepw
98 ine and D-serine (DS), the partial agonist D-cycloserine (DCS) and the antagonist 5,7-dichlorokynuren
102 effects of enhancing NMDAR signaling using d-cycloserine (DCS) on a recently developed LTP EEG paradi
103 ear evidence for an augmentation effect of D-cycloserine (DCS) on exposure therapy for anxiety disord
104 ory processes, whereas the partial agonist D-cycloserine (DCS) potentiates both learning and extincti
105 ficacy of augmenting behavior therapy with D-cycloserine (DCS) to reduce tic severity in a placebo-co
106 rt here that inactivation of the predicted d-cycloserine (DCS) transporter gene cycA resensitized met
108 nxiety disorders, the supplementary use of D-cycloserine (DCS), a partial agonist at the glutamatergi
110 tracellular Mg2+ concentration or applying d-cycloserine (DCS), a partial agonist of the GluN glycine
114 nction have resulted in the development of d-cycloserine (DCS), a partial glutamatergic N-methyl-D-as
116 riments with rat subjects examined whether D-cycloserine (DCS), a partial NMDA agonist, facilitates t
117 hydrocortisone (HC), a corticosteroid, and D-Cycloserine (DCS), an N-methyl-D-aspartate receptor part
119 ive efficacies of NR1 agonists glycine and d-cycloserine (DCS), and found efficacy to be dependent on
120 s to determine if a novel pharmacotherapy, D-cycloserine (DCS), enhanced the efficacy of the psychoth
121 studies for three pharmacological agents [d-cycloserine (DCS), glucocorticoids (GCs), and L-DOPA] wi
122 of the glycineB receptor partial agonist, D-cycloserine (DCS), has been shown to enhance the consoli
123 RSA) can be enhanced by the alanine analog d-cycloserine (DCS), which blocks alanine racemase (Alr1)
129 either NMDA receptor agonists/antagonists (D-cycloserine/dextromethorphan), dopamine type 2 receptor
132 D-aspartate receptor modulators (ketamine, D-cycloserine), electroconvulsive therapy, and transcrania
133 analyses, alprazolam impaired recovery and D-cycloserine enhanced virtual reality outcome in patients
142 ical response were higher in the iTBS plus D-cycloserine group than in the iTBS plus placebo group (7
143 ly more improved at mid-treatment, and the D-cycloserine group's depressive symptoms were significant
146 These results show that at low doses, D-cycloserine has cognition-enhancing properties in this m
149 ursodeoxycholic acid, tryptophan, L-valine, cycloserine, hypoxanthine, and 4-O-Methylmelleolide conc
151 tive symptoms, whereas the partial agonist D-cycloserine improved negative symptoms of patients takin
156 f the transaminase pathway) in the case of d-cycloserine, in contrast to results obtained using the w
160 transport, whereas d-alanine, glycine, and d-cycloserine inhibit CycA-mediated d-serine transport.
164 y results suggest that neither glycine nor D-cycloserine is a generally effective therapeutic option
170 We have shown that cell wall stress (e.g. d-cycloserine) is a potent inducer of the algD operon.
171 is clinical trial indicate that adjunctive D-cycloserine may be a promising strategy for enhancing tr
172 erate to high CSF penetration, linezolid and cycloserine may be effective drugs for TBM treatment, wh
173 onists or antagonists, namely (+/-)HA-966, D-cycloserine, MDL-29,951, DPCQ, MNQX or L-701 252 were ab
175 odulators are covered, including D-serine, D-cycloserine, memantine, and glycine and first-generation
176 oligonucleotides covalently attached to a D-cycloserine molecule, whereby entry into the mycobacteri
177 stant to amikacin, bedaquiline, clofazimine, cycloserine, moxifloxacin, and pyrazinamide, while it in
179 rsely, inhibitors of ceramide biosynthesis L-cycloserine, myriocin and ARN14494 reduced ceramide prod
180 esis via serine palmitoyl-CoA transferase (L-cycloserine, myriocin or ARN14494) were used as a therap
181 either 250 mg of the partial NMDA agonist d-cycloserine (n=20) or matching placebo capsules (n=27).
183 There was a significant dose effect of D-cycloserine on scores on the Scale for the Assessment of
186 re, we examined the impact of D-serine and D-cycloserine on this aversion-resistant alcohol intake (t
188 of virtual reality exposure augmented with D-cycloserine or alprazolam, compared with placebo, in red
189 ol (as compared to ethambutol alone) or as D-cycloserine or biotin covalent adducts without the prese
192 were randomly assigned to receive 50 mg of D-cycloserine or placebo 1 hour before each of five exposu
194 ur E. coli strains exposed to ciprofloxacin, cycloserine, or nitrofurantoin and identify 812 resistan
195 ized clinical trial of adjunctive glycine, D-cycloserine, or placebo conducted at four sites in the U
197 al Impressions-Severity indicated that the d-cycloserine plus CBT group and the placebo plus CBT grou
202 A966 and clonidine, but not propranolol or D-cycloserine, prevented FG7142-associated spatial working
203 The improvement of negative symptoms with D-cycloserine previously observed in patients receiving ty
204 alanine:D-alanine ligase by the antibiotic D-cycloserine proceeds via a distinct phosphorylated form
206 he SANS total score for patients receiving D-cycloserine relative to patients receiving placebo.
210 overproduction is a potential mechanism of D-cycloserine resistance in clinical isolates of M. tuberc
211 results show that one of the mechanisms of D-cycloserine resistance in M. smegmatis involves the over
212 To analyze the genetic determinants of D-cycloserine resistance in mycobacteria, a library of a r
214 st that the ultra-low rate of emergence of D-cycloserine resistance mutations is the dominant biologi
218 ing NMDAR function with the NMDAR co-agonist cycloserine reversed electrophysiological and behavioral
222 Finally, the substrate reduction drug L-cycloserine significantly decreased the level of the pro
223 ne in a multicopy vector were resistant to D-cycloserine, suggesting that AlrA overproduction is a po
224 resulted in poor induction of PalgD-cat by D-cycloserine, suggesting that it also plays a role in the
225 atic assays using recombinant proteins and D-cycloserine susceptibility indicate that the A365V mutat
229 ation of the NMDA receptor partial agonist D-cycloserine, under the same behavioural conditions, did
230 posed to low concentrations of fosfomycin, d-cycloserine, vancomycin, and nisin, indicating a wide-sp
231 nd, placebo-controlled trial investigating D-cycloserine versus placebo augmentation of behavior ther
235 with glycine, l-alanine, l-norvaline, and l-cycloserine was performed by pre-steady-state stopped-fl
241 nd ddl7 conferred high level resistance to D-cycloserine when expressed in Escherichia coli with ddl7
243 activity was partially (64%) inhibited by D-cycloserine, whereas host alanine racemase activity was
244 which blocks palmitoyl-CoA synthesis, and L-cycloserine, which blocks SPT activity, completely block
245 SRT experiments in the Twi mouse utilized l-cycloserine, which inhibits an enzyme several steps upst
246 ound that overlapped with genes induced by d-cycloserine, which is known to activate algD expression.