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 ising method for decreasing relapse in human addicts.
2 therapies for cue-induced relapse in cocaine addicts.
3 ing is a major cause of relapse in abstinent addicts.
4 uce cue-induced relapse in abstinent cocaine addicts.
5 w is bad is a major challenge for recovering addicts.
6 ing deficits of cognitive control in cocaine addicts.
7 potential to reduce relapse in human cocaine addicts.
8 l of cue-elicited craving in abstinent human addicts.
9 induced cocaine craving in abstinent cocaine addicts.
10 s that underlie craving and relapse in human addicts.
11 eterminants of relapse in recovering cocaine addicts.
12 t for previously unresponsive chronic heroin addicts.
13 l and therefore subsequent relapse in opiate addicts.
14 limited by a high relapse rate in abstinent addicts.
15 s aspects of compulsive drug intake in human addicts.
16 gesia and is the main cause of death in drug addicts.
17 k of continued drug seeking and use in human addicts.
18 the nucleus accumbens of male human cocaine addicts.
19 l for recovering cocaine and methamphetamine addicts.
20 he restoration of cognitive function in meth addicts.
21 ulnerability to craving and relapse in human addicts.
22 is a major trigger for relapse in abstinent addicts.
23 cription to which cancer cells become highly addicted.
24 y a small percentage of alcohol users become addicted.
25 ic driver mutations to which tumor cells are addicted.
26 genetic lesion to which the cancer cells are addicted.
27 confirming that these tumors remain oncogene addicted.
28 stress than those of individuals who are not addicted.
31 ion between resting and activation but also 'addicts' active T cells to certain metabolic pathways in
32 Reduced effortful attention performance in addicts also correlated with thinner paralimbic cortices
35 ne expression changes common to both cocaine-addicted and alcoholic individuals that may reflect neur
36 pplying the monetary incentive delay task in addicted and at-risk adult populations are reviewed, wit
38 strate that the CML stem cell is not BCR-ABL addicted and have important implications for developing
39 ions and socioeconomic disadvantage are more addicted and less likely to quit and experience greater
40 d state to which the tumor cells have become addicted and make them vulnerable to therapies and targe
45 st that primitive CML cells are not oncogene addicted and that therapies that biochemically target BC
47 e markers to measure African ancestry in 407 addicts and 457 comparison subjects self-identified as A
48 ated cues trigger relapse to drug seeking in addicts and animals exposed to addictive drugs, even aft
49 opiate withdrawal contributes to relapse in addicts and can be studied in rats by using the opiate w
50 ential harmful effects of DCS-coupled CET in addicts and describe how these concerns might be mitigat
55 ul motivational control over the behavior of addicts, and can contribute to relapse via multiple, dis
56 Even after prolonged periods of abstinence, addicts are at risk of relapse, particularly when cues e
59 uggest that brain structure abnormalities in addicts are related in part to drug use and in part to p
61 (including reward-associated cues), putting addicts at increasing risk to relapse as addiction incre
62 cocaine exposure are responsible for cocaine-addicted behaviors, the underlying molecular mechanism a
63 is a key adaptation occurring in the cocaine-addicted brain, but the effect of cocaine on the fundame
67 ontributors to relapse in recovering cocaine addicts, but the mechanisms by which they influence moti
68 es that showed enhanced ability to kill PI3K-addicted cancer cells and to inhibit Akt phosphorylation
69 ng incomplete tumor cell killing in oncogene-addicted cancer cells, we investigated the role of EGFR
71 We found that many drug-treated "oncogene-addicted" cancer cells engage a positive feedback loop l
72 that targeting nutrient metabolism in energy-addicted cancers with high mTORC1 signaling may be an ef
73 mors, suggesting that treatment of glutamine-addicted cancers with mTOR inhibitors might have benefic
74 nd [hepatocyte growth factor receptor (MET)] addicted cancers, and reactivation of ErbB3 is a promine
75 d PHA-665752, suppressed the growth of c-MET-addicted cancers, but not the growth of cancers that are
79 rols, we hypothesized and found that cocaine-addicted carriers of a 9R-allele exhibited higher respon
80 ion as a mechanism of cell death in oncogene-addicted cells and establish Par-4 as a negative regulat
81 w that despite increased glucose uptake, GLN addicted cells do not metabolize glucose via the TCA cyc
84 Consequently, ABT-263 failed to kill BCL-XL-addicted cells with low activator BH3s and BCL-XL overab
85 nges following drug treatment of mutant EGFR-addicted cells, we identified the stem cell transcriptio
90 ce self-administration paradigm to identify 'addicted' cocaine-preferring (CP) individuals and resist
91 sults suggest a strategy in which recovering addicts could use a systemically active compound to prot
93 also promotes counterselection of NF-kappaB-addicted DLBCL lines by a dual mechanism involving kinas
98 nical observations imply that female cocaine addicts experience enhanced relapse vulnerability compar
99 rose seeking, and may explain the difficulty addicts experience in managing relapse to cocaine use.
105 ethod reveals that the response of 'oncogene-addicted' human cancer cells to tyrosine kinase inhibito
109 oral dependent variables in 73 human cocaine-addicted individuals and 47 healthy controls, we hypothe
111 ug abstinence is frequently compromised when addicted individuals are re-exposed to environmental sti
112 uring cognitive processing characterize drug addicted individuals as compared with healthy controls.
113 ioral trait frequently seen not only in drug-addicted individuals but also in individuals who patholo
115 explanation for the puzzling question of why addicted individuals continue drug consumption despite n
117 ned cues (stimuli associated with the drug), addicted individuals experience an intense desire for th
118 trate fMRI response to drug words in cocaine-addicted individuals in mesencephalic regions as possibl
119 ntions to change the maladaptive behavior of addicted individuals mainly rely on psychosocial approac
121 een 1 month and 6 months of abstinence, when addicted individuals may be most vulnerable to, and perh
122 in prescription opiates may reduce harm, but addicted individuals may switch to other opiates such as
124 umption opportunities, are inappropriate for addicted individuals seeking treatment or abstaining.
125 ng positive for cocaine in urine, 26 cocaine addicted individuals testing negative for cocaine in uri
127 dered neurobiology in a minority of severely addicted individuals, which undermines the implementatio
131 ction, the only effective treatment for many addicts is contingency management, a behavioral treatmen
136 ependent IL-6 secretion unleashed previously addicted lung tumor cells from their EGFR dependency.
140 because of hyperresponsiveness to food cues, addicts may relapse following exposure to their drug of
142 ion-related measures identified a subset of "addicted" mice ( approximately 19%) that exhibited inten
144 f habitual behaviors, evidence suggests that addicts must be very creative and flexible when trying t
146 ere performed in 66 people, involving a food-addicted obese group, a non-food addicted obese group an
147 However food-addicted differ from non-food-addicted obese people by opposite activity in the anteri
148 Brain activity in food-addicted and non-food-addicted obese people is compared to alcohol-addicted an
150 However, to procure such drugs as cocaine, addicts often require considerable ingenuity and flexibi
151 ), indicating that, e.g., astrocytes in drug addicts on average exhibit significant elongation of fib
153 -glutamine levels in the striatum of cocaine-addicted participants (n = 15) compared with healthy con
154 r p63-driven paracrine FGFR2 signaling as an addicting pathway in human cancer and suggest a new appr
155 f principle that targeting multiple oncogene addicted pathways can prevent therapeutic resistance.
156 Positron emission tomography studies in drug-addicted patients have shown that exposure to drug-relat
157 Here we report on impairments in cocaine-addicted patients to act purposefully toward a given goa
161 e examined its role in the development of an addicted phenotype in intact male and female rats, and i
165 are sex differences in the magnitude of the addicted phenotype under optimized conditions that induc
166 e less cocaine exposure before developing an addicted phenotype with evidence implicating estradiol a
167 additional measure for the development of an addicted phenotype, separate groups of rats were screene
168 e an enhanced vulnerability to developing an addicted phenotype, they may be similar to males once ad
169 tration, both males and females developed an addicted phenotype, with 9 of 11 males and 8 of 10 femal
172 across abstinent, recreationally using, and addicted populations demonstrate complexities in interpr
176 ibits miR-155 and slows the growth of these "addicted" pre-B-cell tumors in vivo, suggesting a promis
178 om California who were enrolled in the Civil Addict Program from 1962 onward by use of a natural hist
179 986 that cue-induced drug craving in cocaine addicts progressively increases over the first several w
180 y smaller among cocaine, opiate, and alcohol addicts (proportion=0.76-0.78) than nonaddicted African
182 ferential DNA hydroxymethylation observed in addicted rats occurred mostly at intergenic sites locate
188 elieved that addictive drugs often render an addict's brain reward system hypersensitive, leaving the
189 -associated cues have profound effects on an addict's emotional state and drug-seeking behavior.
190 of the BCR-ABL kinase transforms cells to an addicted state that requires glucose metabolism for surv
196 ested during early or protracted withdrawal, addicted subjects show lower levels of D2 receptors in s
198 effects but have unexpectedly shown that in addicted subjects, drug-induced DA increases (as well as
201 aFosB and CaMKII in the NAc of human cocaine addicts, suggesting possible targets for future therapeu
202 targeting non-oncogenes to which cancers are addicted supports the future development and potential a
203 bey and colleagues describe a unique antigen-addicted T cell population bearing characteristics of bo
206 wed expression changes in alcoholics/cocaine addicts; these factors included genes involved in GABA s
209 proneural" and "classical" subtypes that are addicted to aberrant signaling from integrin alphavbeta3
210 based on the assumption that PDAC cells are addicted to activated KRAS, but this assumption remains
211 question the degree to which PDAC cells are addicted to activated KRAS, by illustrating adaptive non
213 -resolution structural images of 42 patients addicted to alcohol and 32 healthy control participants.
221 vide further evidence that myeloma cells are addicted to c-MYC activity and that c-MYC is a promising
222 g, and Participants: Seventy-six individuals addicted to cocaine with varying durations of abstinence
227 t cells transformed by oncogenic RasV12 were addicted to DDX5, because reduction of DDX5 was sufficie
228 this difficulty, a cancer cell often becomes addicted to DNA repair pathways other than the one that
229 dual differences in the propensity to become addicted to drugs, leading to the description of addicti
232 e large B cell lymphomas (DLBCLs) are mostly addicted to EZH2 but not the more differentiated activat
233 tant plus c-Myc appeared to be become highly addicted to FGFR-dependent prosurvival activities, as sm
235 d metabolism, rendering the transformed cell addicted to glucose for the maintenance of survival.
236 tumour cells are more proliferative but not addicted to HER2, consistent with activation of multiple
237 kinases and the reason why some kinases are addicted to Hsp90 while closely related family members a
238 Here we show that ALCLs of both subtypes are addicted to IRF4 signaling, as knockdown of IRF4 by RNA
239 ata demonstrate that miR-125a-induced MPN is addicted to its sustained overexpression, and highlight
240 n the degree to which pancreatic cancers are addicted to KRAS by illustrating adaptive nongenetic and
242 we demonstrated that MYC-induced tumors are addicted to mutant beta-catenin, and the combined inacti
245 ma (DLBCL) is an aggressive lymphoma that is addicted to NF-kappaB signaling through the CARD11-BCL10
246 who think them safe or by those sufficiently addicted to nicotine to not be able to quit e-cigarette
249 results demonstrate that tumours can become addicted to oncomiRs and support efforts to treat human
250 annabis users progress to using and becoming addicted to other drugs, but the reasons for this progre
255 PI3K/AKT-dependent GCB DLBCL subtype that is addicted to PI3K and MYC signaling and suggest that phar
259 utant allelic ratios and, in vitro, are more addicted to the aberrant signaling from the FLT3/ITD onc
261 RBB2-amplified breast tumour lines are truly addicted to the ERBB2 oncogene at the mRNA level and dis
263 large B-cell lymphoma (DLBCL) cell lines are addicted to the expression of OCT2 and its coactivator O
265 d that tumor cells carrying a mutant p53 are addicted to the mutant for cell survival and resistance
266 carcinoma cells that carry a mutant p53, are addicted to the mutant for their survival and resistance
268 gy enables melanomas that would otherwise be addicted to the Ras-Raf pathway to instead tolerate path
269 tablished that glioblastomas are selectively addicted to this pathway as a strategy to evade oncogene
271 on learning, however, impairs the ability of addicts to generalize extinction training to the drug-ta
273 a failure of the brain mechanisms that allow addicts to learn about and mentally simulate non-drug co
274 cci with high transformation capability are "addicted" to a "hypertransformable" state for optimal fi
276 gly, MYCN-amplified neuroblastoma cells are "addicted" to LDHA enzymatic activity, as its depletion c
277 ors displaying c-MET gene amplification are "addicted" to MET signaling and therefore are very sensit
279 on-small cell lung cancer (NSCLC) cells are 'addicted' to basal autophagy that reprograms cellular me
280 tumour cells expressing activated AKT1 are 'addicted' to FoxM1, as they require continuous presence
281 recent findings suggest that tumors can be 'addicted' to miRNA overexpression, yielding a possible t
282 hese genetic aberrations cause tumors to be 'addicted' to NF-kappaB, which can be exploited therapeut
284 Notably, increased NRP2 expression in EGFR-addicted tumor cells led to downregulation of EGFR prote
285 er, STK38 knockdown suppresses growth of MYC-addicted tumors in vivo, thus providing a novel viable t
286 er, STK38 knockdown suppresses growth of MYC-addicted tumors in vivo, thus providing a novel viable t
289 cement theories of drug addiction posit that addicts use drugs to alleviate negative mood states.
290 morphology of hippocampal astrocytes in drug addicts versus controls and further supports the involve
292 cue-elicited craving among detoxified heroin addicts was substantially attenuated following R-E train
293 recipitates drug-seeking behavior in cocaine addicts, we also postulated that cocaine manifests its e
294 To better model drug-seeking behavior in addicts, we first developed a novel cocaine self-adminis
297 ral and connectivity changes in the brain of addicts which appear permanent, making control of learne
298 controlled trial, we enrolled chronic heroin addicts who were receiving conventional oral treatment (
WebLSDに未収録の専門用語（用法）は "新規対訳" から投稿できます。