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 l for recovering cocaine and methamphetamine addicts.
2 ce may foster maladaptive nicotine taking in addicts.
3 he restoration of cognitive function in meth addicts.
4 ulnerability to craving and relapse in human addicts.
5 is a major trigger for relapse in abstinent addicts.
6 ising method for decreasing relapse in human addicts.
7 therapies for cue-induced relapse in cocaine addicts.
8 ing is a major cause of relapse in abstinent addicts.
9 uce cue-induced relapse in abstinent cocaine addicts.
10 w is bad is a major challenge for recovering addicts.
11 ing deficits of cognitive control in cocaine addicts.
12 effective treatment strategies for inhalant addicts.
13 potential to reduce relapse in human cocaine addicts.
14 l of cue-elicited craving in abstinent human addicts.
15 induced cocaine craving in abstinent cocaine addicts.
16 s that underlie craving and relapse in human addicts.
17 eterminants of relapse in recovering cocaine addicts.
18 enders are as high as relapse rates for drug addicts.
19 ng factors for psychiatric-illnesses in METH addicts.
20 the nucleus accumbens of male human cocaine addicts.
21 k of continued drug seeking and use in human addicts.
22 y a small percentage of alcohol users become addicted.
23 ic driver mutations to which tumor cells are addicted.
24 genetic lesion to which the cancer cells are addicted.
25 confirming that these tumors remain oncogene addicted.
26 d by mutant p53 to which cancer cells become addicted.
27 cription to which cancer cells become highly addicted.
29 mers (24 +/- 2.8 yrs; 88.64% Male), 30% were addicted, 30% were problematic, 8% were engaged and 32%
31 ion between resting and activation but also 'addicts' active T cells to certain metabolic pathways in
34 ne expression changes common to both cocaine-addicted and alcoholic individuals that may reflect neur
35 pplying the monetary incentive delay task in addicted and at-risk adult populations are reviewed, wit
37 ions and socioeconomic disadvantage are more addicted and less likely to quit and experience greater
38 d state to which the tumor cells have become addicted and make them vulnerable to therapies and targe
44 opiate withdrawal contributes to relapse in addicts and can be studied in rats by using the opiate w
45 ential harmful effects of DCS-coupled CET in addicts and describe how these concerns might be mitigat
50 ., non-problematic, engaged, problematic and addicted) and (3) the predictive power of socioeconomic
51 ul motivational control over the behavior of addicts, and can contribute to relapse via multiple, dis
52 Even after prolonged periods of abstinence, addicts are at risk of relapse, particularly when cues e
56 (including reward-associated cues), putting addicts at increasing risk to relapse as addiction incre
57 cocaine exposure are responsible for cocaine-addicted behaviors, the underlying molecular mechanism a
59 is a key adaptation occurring in the cocaine-addicted brain, but the effect of cocaine on the fundame
63 ontributors to relapse in recovering cocaine addicts, but the mechanisms by which they influence moti
65 es that showed enhanced ability to kill PI3K-addicted cancer cells and to inhibit Akt phosphorylation
66 ng incomplete tumor cell killing in oncogene-addicted cancer cells, we investigated the role of EGFR
68 We found that many drug-treated "oncogene-addicted" cancer cells engage a positive feedback loop l
70 that targeting nutrient metabolism in energy-addicted cancers with high mTORC1 signaling may be an ef
71 mors, suggesting that treatment of glutamine-addicted cancers with mTOR inhibitors might have benefic
72 d PHA-665752, suppressed the growth of c-MET-addicted cancers, but not the growth of cancers that are
73 s show efficacy in preclinical models of Wnt-addicted cancers, including RNF43-mutant pancreatic canc
74 e have previously shown that, unlike glucose-addicted cancers, Kaposi's sarcoma-associated herpesviru
80 rols, we hypothesized and found that cocaine-addicted carriers of a 9R-allele exhibited higher respon
81 ighly effective to inhibit the growth of RTK-addicted cell lines and hepatocellular (HCC) cells in vi
82 ion as a mechanism of cell death in oncogene-addicted cells and establish Par-4 as a negative regulat
83 w that despite increased glucose uptake, GLN addicted cells do not metabolize glucose via the TCA cyc
85 Consequently, ABT-263 failed to kill BCL-XL-addicted cells with low activator BH3s and BCL-XL overab
86 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
94 also promotes counterselection of NF-kappaB-addicted DLBCL lines by a dual mechanism involving kinas
100 nical observations imply that female cocaine addicts experience enhanced relapse vulnerability compar
101 rose seeking, and may explain the difficulty addicts experience in managing relapse to cocaine use.
104 previous studies, reporting problematic and addicted gamers show poorer health outcomes compared wit
105 t overexpresses miR-155 and develops miR-155-addicted hematological malignancy, we describe here a mu
109 ethod reveals that the response of 'oncogene-addicted' human cancer cells to tyrosine kinase inhibito
110 increased relapse-like behavior, and, as in addicted humans, major increases in opioid economic dema
113 oral dependent variables in 73 human cocaine-addicted individuals and 47 healthy controls, we hypothe
114 ug abstinence is frequently compromised when addicted individuals are re-exposed to environmental sti
115 ioral trait frequently seen not only in drug-addicted individuals but also in individuals who patholo
117 explanation for the puzzling question of why addicted individuals continue drug consumption despite n
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
123 umption opportunities, are inappropriate for addicted individuals seeking treatment or abstaining.
125 dered neurobiology in a minority of severely addicted individuals, which undermines the implementatio
128 ction, the only effective treatment for many addicts is contingency management, a behavioral treatmen
134 ng SCARB1 with HDL NPs in cholesterol uptake-addicted lymphoma cells abolishes GPX4, resulting in can
137 in a subpopulation of SIV-infected morphine addicted macaques, the presence of drugs of abuse may ca
138 rus (SIV) infections in control and morphine-addicted macaques, we found that two of the most signifi
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
145 As a result, adoptive transfer of such IL-15-addicted NK cells is associated with cellular stress bec
147 ere performed in 66 people, involving a food-addicted obese group, a non-food addicted obese group an
148 However food-addicted differ from non-food-addicted obese people by opposite activity in the anteri
149 Brain activity in food-addicted and non-food-addicted obese people is compared to alcohol-addicted an
151 However, to procure such drugs as cocaine, addicts often require considerable ingenuity and flexibi
152 ), indicating that, e.g., astrocytes in drug addicts on average exhibit significant elongation of fib
154 H-Ras signal output and the growth of K-Ras-addicted pancreatic and non-small cell lung cancer cells
156 -glutamine levels in the striatum of cocaine-addicted participants (n = 15) compared with healthy con
157 r p63-driven paracrine FGFR2 signaling as an addicting pathway in human cancer and suggest a new appr
158 f principle that targeting multiple oncogene addicted pathways can prevent therapeutic resistance.
159 Here we report on impairments in cocaine-addicted patients to act purposefully toward a given goa
162 e examined its role in the development of an addicted phenotype in intact male and female rats, and i
166 are sex differences in the magnitude of the addicted phenotype under optimized conditions that induc
167 e less cocaine exposure before developing an addicted phenotype with evidence implicating estradiol a
168 additional measure for the development of an addicted phenotype, separate groups of rats were screene
169 e an enhanced vulnerability to developing an addicted phenotype, they may be similar to males once ad
170 tration, both males and females developed an addicted phenotype, with 9 of 11 males and 8 of 10 femal
174 across abstinent, recreationally using, and addicted populations demonstrate complexities in interpr
179 unctioning have been observed in healthy and addicted populations; however, there is limited evidence
180 ibits miR-155 and slows the growth of these "addicted" pre-B-cell tumors in vivo, suggesting a promis
182 om California who were enrolled in the Civil Addict Program from 1962 onward by use of a natural hist
183 986 that cue-induced drug craving in cocaine addicts progressively increases over the first several w
185 ferential DNA hydroxymethylation observed in addicted rats occurred mostly at intergenic sites locate
190 elieved that addictive drugs often render an addict's brain reward system hypersensitive, leaving the
191 -associated cues have profound effects on an addict's emotional state and drug-seeking behavior.
192 of the BCR-ABL kinase transforms cells to an addicted state that requires glucose metabolism for surv
198 ptor tyrosine kinase inhibitors for oncogene-addicted subgroups of non-small-cell lung cancer (for ex
199 ested during early or protracted withdrawal, addicted subjects show lower levels of D2 receptors in s
201 effects but have unexpectedly shown that in addicted subjects, drug-induced DA increases (as well as
205 aFosB and CaMKII in the NAc of human cocaine addicts, suggesting possible targets for future therapeu
206 bey and colleagues describe a unique antigen-addicted T cell population bearing characteristics of bo
209 ts while ensuring that other products do not addict the next generation of youth and adolescents.
210 wed expression changes in alcoholics/cocaine addicts; these factors included genes involved in GABA s
213 proneural" and "classical" subtypes that are addicted to aberrant signaling from integrin alphavbeta3
214 based on the assumption that PDAC cells are addicted to activated KRAS, but this assumption remains
215 question the degree to which PDAC cells are addicted to activated KRAS, by illustrating adaptive non
217 -resolution structural images of 42 patients addicted to alcohol and 32 healthy control participants.
222 trast, using an Myc-dependent leukemic model addicted to autophagy, we show that knockdown of Grasp55
226 vide further evidence that myeloma cells are addicted to c-MYC activity and that c-MYC is a promising
227 bitors, approved for a breast cancer subtype addicted to CDK4/6 activation, could be repurposed to tr
229 g, and Participants: Seventy-six individuals addicted to cocaine with varying durations of abstinence
233 t cells transformed by oncogenic RasV12 were addicted to DDX5, because reduction of DDX5 was sufficie
234 this difficulty, a cancer cell often becomes addicted to DNA repair pathways other than the one that
235 dual differences in the propensity to become addicted to drugs, leading to the description of addicti
237 e large B cell lymphomas (DLBCLs) are mostly addicted to EZH2 but not the more differentiated activat
238 o understand which cancers are oncogenically addicted to FGF19 amplification as well as the role it s
239 hondrial dysfunction, TOP1MT-KO cells become addicted to glycolysis, which limits synthetic building
240 tumour cells are more proliferative but not addicted to HER2, consistent with activation of multiple
241 kinases and the reason why some kinases are addicted to Hsp90 while closely related family members a
242 Here we show that ALCLs of both subtypes are addicted to IRF4 signaling, as knockdown of IRF4 by RNA
243 ata demonstrate that miR-125a-induced MPN is addicted to its sustained overexpression, and highlight
244 n the degree to which pancreatic cancers are addicted to KRAS by illustrating adaptive nongenetic and
246 Cells with BRAF(V600E) amplification are addicted to MEKi to maintain a precise level of ERK1/2 s
247 we demonstrated that MYC-induced tumors are addicted to mutant beta-catenin, and the combined inacti
248 tion for treating pancreatic tumors that are addicted to mutant KRAS, thus offering opportunities for
251 ma (DLBCL) is an aggressive lymphoma that is addicted to NF-kappaB signaling through the CARD11-BCL10
252 who think them safe or by those sufficiently addicted to nicotine to not be able to quit e-cigarette
255 ous diseases in people who misuse and/or are addicted to opioids and to concurrently address the unde
256 phase 3, randomised trial with men and women addicted to opioids who were starting antiretroviral the
257 annabis users progress to using and becoming addicted to other drugs, but the reasons for this progre
262 PI3K/AKT-dependent GCB DLBCL subtype that is addicted to PI3K and MYC signaling and suggest that phar
266 utant allelic ratios and, in vitro, are more addicted to the aberrant signaling from the FLT3/ITD onc
268 RBB2-amplified breast tumour lines are truly addicted to the ERBB2 oncogene at the mRNA level and dis
269 large B-cell lymphoma (DLBCL) cell lines are addicted to the expression of OCT2 and its coactivator O
271 d that tumor cells carrying a mutant p53 are addicted to the mutant for cell survival and resistance
273 gy enables melanomas that would otherwise be addicted to the Ras-Raf pathway to instead tolerate path
274 tablished that glioblastomas are selectively addicted to this pathway as a strategy to evade oncogene
276 on learning, however, impairs the ability of addicts to generalize extinction training to the drug-ta
277 a failure of the brain mechanisms that allow addicts to learn about and mentally simulate non-drug co
278 cci with high transformation capability are "addicted" to a "hypertransformable" state for optimal fi
279 ors displaying c-MET gene amplification are "addicted" to MET signaling and therefore are very sensit
280 on-small cell lung cancer (NSCLC) cells are 'addicted' to basal autophagy that reprograms cellular me
281 hese genetic aberrations cause tumors to be 'addicted' to NF-kappaB, which can be exploited therapeut
283 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
290 cement theories of drug addiction posit that addicts use drugs to alleviate negative mood states.
291 morphology of hippocampal astrocytes in drug addicts versus controls and further supports the involve
293 cue-elicited craving among detoxified heroin addicts was substantially attenuated following R-E train
294 recipitates drug-seeking behavior in cocaine addicts, we also postulated that cocaine manifests its e
295 To better model drug-seeking behavior in addicts, we first developed a novel cocaine self-adminis
298 ral and connectivity changes in the brain of addicts which appear permanent, making control of learne