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1 ber structure in Ada(-/-) mice post two-week drug withdrawal.
2 on at week 54, and adverse events leading to drug withdrawal.
3 ients and their providers about an important drug withdrawal.
4  the antagonist MK801, and accelerates after drug withdrawal.
5 prognostic value in predicting relapse after drug withdrawal.
6 adaptations remain unopposed and may lead to drug withdrawal.
7 ment in myocardial pathology after inotropic drug withdrawal.
8 e peripheral and is usually reversible after drug withdrawal.
9 imals ultimately rejected their grafts after drug withdrawal.
10 es and became most pronounced upon prolonged drug withdrawal.
11 ndary motoneurons that is not ameliorated by drug withdrawal.
12 of 1 or more black box warnings per drug, or drug withdrawal.
13 ly) that returned to preinduction size after drug withdrawal.
14 and MEKi resistance are reversible following drug withdrawal.
15 oliferation persisted for several days after drug withdrawal.
16 duced graft survival after immunosuppressive drug withdrawal.
17 e performed serially for up to 10 days after drug withdrawal.
18 evelopment as well as residual effects after drug withdrawal.
19 on at week 54, and adverse events leading to drug withdrawal.
20 recovery was evident within 3 days following drug withdrawal.
21 nded to either immunomodulating therapies or drug withdrawal.
22 tensity of cue-induced cocaine seeking after drug withdrawal.
23 k fitness exhibit dynamic transcription upon drug withdrawal.
24 newal capacity that mediated cGVHD following drug withdrawal.
25 ms leading to psoriasis recurrence following drug withdrawal.
26 ble for cells to reenter the cell cycle upon drug withdrawal.
27 s is due to chronic effects, ongoing use, or drug withdrawal.
28 ibuting to cocaine craving and relapse after drug withdrawal.
29 dministration and lasts throughout prolonged drug withdrawal.
30 cited a sustained replication response after drug withdrawal.
31  largely reversible upon Cdk9 restoration or drug withdrawal.
32 to promote cue-induced cocaine seeking after drug withdrawal.
33 th treatment (P = 0.001) and decreased after drug withdrawal.
34    Striatal changes reversed within weeks of drug withdrawal.
35 with the hepatotoxicity that has resulted in drug withdrawal.
36 of antidepressants on Ga (s) signaling after drug withdrawal.
37 nd transcriptional changes that persist upon drug withdrawal.
38 pletion, and observe GAMM repopulation after drug withdrawal.
39 d, minimizing transcriptional reversion upon drug withdrawal.
40 109/L or less leading to a dose reduction or drug withdrawal.
41  on the negative affective state after acute drug withdrawal.
42 g calcium-permeable AMPARs (CP-AMPARs) after drug withdrawal.
43 relapse effects of EE can be unleashed after drug withdrawal.
44 tients were evaluated for 12 months or until drug withdrawal.
45 ional state may exist between depression and drug withdrawal.
46 ) and elicits negative affective states upon drug withdrawal.
47 levels similar to the healthy controls after drug withdrawal.
48 on symptoms in chronic drug users long after drug withdrawal.
49 ations in reward valuation during protracted drug withdrawal.
50  is unpredictable and almost always leads to drug withdrawal.
51 eizures, an effect that persists weeks after drug withdrawal.
52 nib, 100% of the diseased mice relapsed upon drug withdrawal.
53 ized, prospective study of immunosuppression drug withdrawal.
54 l biopsies performed up to 3 years following drug withdrawal.
55 idepressant effect was still seen 2 wk after drug withdrawal.
56 oing colistin treatment, and upon subsequent drug withdrawal.
57 as been implicated in negative affect during drug withdrawal.
58 duced liver injury (DILI) is a main cause of drug withdrawal.
59 ed to durable antitumor responses even after drug withdrawal.
60 lammation and also ameliorate the effects of drug withdrawal.
61 l population, an effect that was reversed on drug withdrawal.
62 gic EPSC frequency persisted 10-20 min after drug withdrawal.
63 owed regrowth of the tumor vasculature after drug withdrawal.
64  seizure susceptibility, a common symptom of drug withdrawal.
65 tological features should be normal prior to drug withdrawal.
66 and neural consequences following 2 weeks of drug withdrawal.
67  Drd1-EGFP-positive neurons after 30 days of drug withdrawal.
68  predictive of the viral RNA set point after drug withdrawal.
69  in Drd1-EGFP-positive neurons 30 days after drug withdrawal.
70 safety concerns, clinical trial failures and drug withdrawals.
71 eases in development costs, and high-profile drug withdrawals.
72                                        After drug withdrawal, a key factor triggering relapse is prog
73   Following abrupt BUP/SAM discontinuation, "drug withdrawal" AEs were infrequent (0.4%), and the inc
74 rable progress has been made in achieving IS drug withdrawal after cell therapy in recipients of orga
75 , seizure-free interval before antiepileptic drug withdrawal, age at onset of epilepsy, history of fe
76  with acute and chronic drug misuse and with drug withdrawal and abstinence sequelae.
77  blood samples obtained before initiation of drug withdrawal and at rejection, alongside blood sample
78 2 T cell recovery correlated with time since drug withdrawal and inversely correlated with patient ag
79 eloped fluid retention, which reversed after drug withdrawal and presented predominantly as periphera
80 t treatment involving alternating periods of drug withdrawal and rechallenge has been proposed as a m
81  the aversive motivational state produced by drug withdrawal and the development of the drug-dependen
82 d by DDC refeeding lasted for 4 months after drug withdrawal and was not manifest when SAMe was added
83 about the mechanism by which MPDZ influences drug withdrawal and/or other CNS hyperexcitability state
84 d into several sections: the first describes drug withdrawals and new general reviews of drug-induced
85       However, psoriasis may recur following drug withdrawal, and as a result, patients tend to conti
86 ntihypertensive agents, in the management of drug withdrawal, and as sedative analgesics.
87 s have just completed or are in the midst of drug withdrawal, and four patients were not withdrawn du
88 pecimens from 27 long-term recipients before drug withdrawal, and from 10 patients with recent transp
89 ls in the viral RNA set point after complete drug withdrawal, and none of the animals was able to ach
90 are an integral part of acute and protracted drug withdrawal, and several lines of evidence have show
91 with heroin delivery, followed by 2 weeks of drug withdrawal, and then reinstated to heroin-condition
92  of +/- cells failed to reach anaphase after drug withdrawal, and those that entered anaphase showed
93  The frequencies of remission, relapse after drug withdrawal, and treatment failure were comparable i
94                              After long-term drug withdrawal (approximately postnatal day 100), we ex
95  on the premise that repeated relapses after drug withdrawal are inevitable.
96             Although long-lasting effects of drug withdrawal are thought to play a key role in motiva
97 e inhibitors (TKIs) underwent apoptosis upon drug withdrawal as a consequence of ERK1/2 hyperactivati
98 rring only with physiological stress such as drug withdrawal) at 2 years and 5 years after surgery on
99 d Drd2-EGFP-positive neurons after 2 days of drug withdrawal but only in Drd1-EGFP-positive neurons a
100 the chromatin structure were reversible upon drug withdrawal, but obligatory for the potentiation of
101 ression converted to sirolimus, and complete drug withdrawal by 24 months post-transplantation.
102 though aLQTS has become the leading cause of drug withdrawal by the U.S.
103  QT syndrome (aLQTS), is a leading cause for drug withdrawal by the United States Food and Drug Admin
104  a prospective multicenter immunosuppressive drug withdrawal clinical trial.
105                                        After drug withdrawal, cocaine-generated silent synapses becam
106  after at least 12 hours of antiparkinsonian drug withdrawal) compared with baseline (ie, prior to th
107 viously implicated in both schizophrenia and drug withdrawal delirium, exhibited frequent replacement
108 cell cycle, and differentiated normally upon drug withdrawal, demonstrating reversibility of the effe
109                Incidence of side-effects and drug withdrawals did not differ by much between the two
110           Second, some patients benefit from drug withdrawal (discontinuation of the overused medicat
111 te (DDC) for 10 weeks followed by 1 month of drug withdrawal (drug-primed mice) and then 7 days of dr
112 emission, time to first seizure, and time to drug withdrawal due to inadequate seizure control or sid
113 rapy, time to 12-month remission, or time to drug withdrawal due to unacceptable side-effects or to l
114                                              Drug withdrawal effects on negative symptom factors were
115 rences in use of medical services or adverse drug withdrawal effects were observed.
116 trate that nicotine exposure, independent of drug withdrawal effects, increases stress sensitivity, a
117  utilization of medical services, or adverse drug withdrawal effects.
118 mes were use of medical services and adverse drug withdrawal effects.
119                                One day after drug withdrawal, endothelial sprouts grew into empty sle
120 d the proportion of patients with an adverse drug withdrawal event (ADWE).
121                              Serious adverse drug withdrawal events involving opioids or sedative-hyp
122 rst 30 days postdischarge (including adverse drug withdrawal events) captured through structured tele
123  facilitate prediction of outcomes following drug withdrawal for the individual patient, including bo
124 us joint-action analysis to investigate poly-drug withdrawal from fixed-ratio cocaine/kappa-opioid ag
125 ver injury (DILI) remains a leading cause of drug withdrawal from human clinical trials or the market
126 re found to be reversible within 24 hours of drug withdrawal from the cell culture media.
127 sible for over 60% of black box warnings and drug withdrawals from the market place in the United Sta
128 re in clinical trials and a major reason for drug withdrawals from the market.
129                         Following 8 weeks of drug withdrawal, HAL-induced changes in brain volumes no
130                        The consequences that drug withdrawal has on immune functioning has only recen
131 on protocols with complete immunosuppressive drug withdrawal have been tested in humans.
132 olecular pathways associated with successful drug withdrawal, however, are not well defined.
133 acement therapy and management of iatrogenic drug withdrawal in ICU patients.
134              Symptom exacerbation induced by drug withdrawal in patients with treatment-resistant sch
135 mental medicine approach of immunomodulatory drug withdrawal in rheumatoid arthritis (RA) remission t
136 induced liver toxicity and the importance of drug withdrawal in the event of liver injury.
137  withdrawal of rofecoxib, one of the largest drug withdrawals in United States history, and instruct
138 (BNST), each of which has been implicated in drug-withdrawal-induced anxiety and stress-induced respo
139 ism underlying the relapse to drug use after drug withdrawal is largely unknown.
140 ssists in identifying those patients in whom drug withdrawal is likely to be unsuccessful and in whom
141 icts that the first step in the induction of drug withdrawal is the activation of reward-related circ
142 epressive effects) in rats and humans (e.g., drug withdrawal, kappa-opioid agonists).
143                      Earlier recognition and drug withdrawal may avoid the serious and sometimes fata
144 ng age and treatment duration, antiepileptic drug withdrawal may be justified.
145                                   Aspects of drug withdrawal may become conditioned to previously neu
146 al output and suggest one mechanism by which drug withdrawal may influence limbic dopamine-dependent
147 ntipsychotic agents and the possibility that drug withdrawal may negatively affect subsequent drug re
148 , seizure-free interval before antiepileptic drug withdrawal, number of antiepileptic drugs before wi
149 icant bradycardia/hypotension, necessitating drug withdrawal, occurred in 2 of 40 (5%) patients on so
150 ee times normal), all of which reversed with drug withdrawal, occurred in five patients (P=.03 vs pla
151            Understanding the consequences of drug withdrawal on immune function and host defense to i
152                         Before initiation of drug withdrawal, operationally tolerant and non-tolerant
153  gaps in knowledge, including the effects of drug withdrawal or dependence on social function or the
154 ommon variation influences either seizure or drug withdrawal outcomes after initiation of antiepilept
155  used negative symptom ratings obtained in a drug withdrawal paradigm to compare symptom profiles in
156 e 29 participants who entered the randomised drug withdrawal period, ten (34%) were female and 19 (66
157 se changes largely resolve by the end of the drug withdrawal period.
158 re in hypertension, reduction in alcohol and drug withdrawal phenomena, reduction in nicotine withdra
159 s prompted a previously reported prospective drug withdrawal program in 59 liver recipients.
160 has been attributed to drug addiction, where drug withdrawal reduces the viability of resistant cells
161                                        After drug withdrawal, reemergence of clonal EGFR mutations on
162 nference, liver for up to 6 months following drug withdrawal required a replication efficiency of at
163 ere unable to complete DNA replication after drug withdrawal, resulting in lethality.
164 A-type glutamate receptors (CP-AMPARs) after drug withdrawal results in profound remodeling of NAc ne
165 seizures, the diagnosis excluding alcohol or drug withdrawal seizures or such recurring exogenous eve
166 orly understood, and strategies for complete drug withdrawal should be selected carefully to avoid gr
167                                        After drug withdrawal, some of these synapses mature by recrui
168                                        After drug withdrawal, some of these synapses mature by recrui
169 changes associated with various psychotropic drug withdrawal states, suggesting a common unifying mec
170                                              Drug-withdrawal stressors, related to long-term pharmaco
171 t of primary NSCLC, and they persisted after drug withdrawal, suggesting the benefits were durable.
172      Drug administration to avoid unpleasant drug withdrawal symptoms has been hypothesized to be a c
173 for alleviating incisional pain and narcotic drug withdrawal symptoms, which are now in clinical tria
174 gs of abuse and the manifestations of opiate/drug withdrawal symptoms.
175 tal abstinence syndrome (NAS) is a postnatal drug withdrawal syndrome primarily caused by maternal op
176 dence of the neonatal abstinence syndrome, a drug-withdrawal syndrome that most commonly occurs after
177 euromuscular blockers, pain assessments, and drug withdrawal syndromes were gathered during the first
178  rigorously tested in comparative studies of drug withdrawal treatment; their use as additional or al
179 ed synapses in the AMPAR-silent state during drug withdrawal, until they were replaced by nonGluN2B N
180 tion confers a selective disadvantage during drug withdrawal, validating intermittent dosing to fores
181                    Disease recurrence during drug withdrawal was documented in 2 of 13 patients with
182 Y/F zidovudine resistance mutation following drug withdrawal were estimated to be 96 to 98% that of t
183           Psychiatric disorders, drug use or drug withdrawal were rarely causally related to RBD.
184 pirin and the kinetics of its recovery after drug withdrawal were similar in patients and control sub
185  expression is dramatically increased during drug withdrawal, which would suggest a direct connection
186                                  Complete IS drug withdrawal without chimerism was reported in a pros
187 imize treatment-outcome where antidepressant drug withdrawal would be problematic.

 
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