ライフサイエンスコーパス: nicotine addiction

1 nular activity may yield approaches to treat nicotine addiction.

2 and are attracting youth to new avenues for nicotine addiction.

3 aptic transmission, synaptic plasticity, and nicotine addiction.

4 ribute to the development and maintenance of nicotine addiction.

5 numbers, which may underlie some aspects of nicotine addiction.

6 are logical candidates for vulnerability to nicotine addiction.

7 for understanding the mechanisms underlying nicotine addiction.

8 ation of dopaminergic pathways implicated in nicotine addiction.

9 eceptors, processes thought to contribute to nicotine addiction.

10 ne and to the development of drugs to combat nicotine addiction.

11 d may have clinical implications in treating nicotine addiction.

12 ol and evaluated its therapeutic efficacy on nicotine addiction.

13 r interventions capable of reliably treating nicotine addiction.

14 r achieving an end to commercial tobacco and nicotine addiction.

15 elaxants that may be repurposed for treating nicotine addiction.

16 to manage several neurological disorders and nicotine addiction.

17 ing CHRNB2 in the brain for the treatment of nicotine addiction.

18 ds and the subcellular mechanisms underlying nicotine addiction.

19 particularly among older midlife adults with nicotine addiction.

20 drawal, providing novel targets for treating nicotine addiction.

21 tanding of neuronal excitability control and nicotine addiction.

22 tors are critical for smoking initiation and nicotine addiction.

23 acetylcholine receptor (nAChR) subunits, to nicotine addiction.

24 It is also the likely receptor that mediates nicotine addiction.

25 promising new approach for the treatment of nicotine addiction.

26 icotine are probably critical for sustaining nicotine addiction.

27 ol processes are a primary characteristic of nicotine addiction.

28 be used in the treatment of lung cancer and nicotine addiction.

29 opment and progression of lung cancer and in nicotine addiction.

30 d up-regulation is believed to contribute to nicotine addiction.

31 ich are therapeutic targets and mediators of nicotine addiction.

32 ping compounds to selectively interfere with nicotine addiction.

33 g rewiring of glutamatergic circuitry during nicotine addiction.

34 immunotherapy may be effective in combating nicotine addiction.

35 en identified as a novel target for managing nicotine addiction.

36 ic stages, and identified new biomarkers for nicotine addiction.

37 k-1, and unc-30 to be potential effectors of nicotine addiction.

38 mice, mGluR5 is suggested to be involved in nicotine addiction.

39 in the CHRNA5-CHRNA3-CHRNB4 gene cluster and nicotine addiction.

40 subunit are associated with vulnerability to nicotine addiction.

41 unique target for therapeutic treatments for nicotine addiction.

42 f nicotine may contribute to the tenacity of nicotine addiction.

43 icated in pathological conditions, including nicotine addiction.

44 that has led to our present understanding of nicotine addiction.

45 olecular, cellular and systems mechanisms of nicotine addiction.

46 nal nAChR, the receptor most associated with nicotine addiction.

47 ebral cortex and white matter structure, and nicotine addiction.

48 pe that is known to play a prominent role in nicotine addiction.

49 other neurotensin receptor agonists to treat nicotine addiction.

50 ysiology and have been clearly implicated in nicotine addiction.

51 resent a new therapeutic target for treating nicotine addiction.

52 ad of cigarettes does not reduce the risk of nicotine addiction; (3) as the number of cigars smoked a

53 everal neuropsychiatric disorders, including nicotine addiction, Alzheimer's, schizophrenia, and depr

54 Nicotine addiction and alcohol use disorders are very wi

55 cco products present a deadly combination of nicotine addiction and carcinogen exposure resulting in

56 ment of therapeutics that target symptoms of nicotine addiction and for theories of addiction.

57 s (e-cigs) among youth raises concerns about nicotine addiction and health risks, highlighting the ur

58 is locus may be a key region associated with nicotine addiction and its treatment.

59 ve linked the chromosome 15q24-25.1 locus to nicotine addiction and lung cancer susceptibility.

60 drugs for modulating nAChR function to treat nicotine addiction and other disorders.

61 e endings where they play important roles in nicotine addiction and Parkinson's disease.

62 ons are important targets for drugs to treat nicotine addiction and Parkinson's disease.

63 1 and its analogues in preclinical models of nicotine addiction and perhaps other disorders involving

64 n and attention, which might be connected to nicotine addiction and probability of relapse in smokers

65 ough methods to help interrupt the spread of nicotine addiction and reduce the downstream morbidity.

66 IC) is thought to be a critical substrate of nicotine addiction and relapse.

67 e therapeutic potential for the treatment of nicotine addiction and several neuropsychiatric disorder

68 may facilitate smoke inhalation and promote nicotine addiction and smoking-related morbidities.

69 her implicates the lateral PFC and insula in nicotine addiction and suggests the use of deep high-fre

70 ults offer new perspectives when considering nicotine addiction and the high prevalence of smoking in

71 million people die from diseases related to nicotine addiction and tobacco use each year.

72 harmacological and biochemical mechanisms of nicotine addiction and tobacco use.

73 gulation has been proposed to play a role in nicotine addiction and withdrawal.

74 , in certain brain areas, may be involved in nicotine addiction and/or withdrawal.

75 ing several types of addiction (most notably nicotine addiction) and other compulsive behaviors.

76 lating neurotransmitter release, reinforcing nicotine addiction, and a role in neurological disorders

77 ophic factor (BDNF) might be associated with nicotine addiction, and circulating BDNF is a biomarker

78 enance of substance abuse, its importance in nicotine addiction, and findings that insular inactivati

79 (nAChRs) is implicated in several aspects of nicotine addiction, and menthol cigarette smokers tend t

80 in the vertebrate nervous system, underlies nicotine addiction, and nicotinic receptor dysfunction l

81 y may serve as a circuit-level biomarker for nicotine addiction, and the development of new therapeut

82 ent, combination or novel drugs, and viewing nicotine addiction as a chronic disorder that might need

83 ciated with both a protective effect against nicotine addiction as a dichotomized trait (Z=-3.04, P<.

84 associated with a protective effect against nicotine addiction as either a dichotomized trait or a q

85 ) could provide new effective treatments for nicotine addiction, as well as other disorders.

86 Nicotine addiction begins with high-affinity binding of

87 class of receptors, potentially important in nicotine addiction, binds alpha-conotoxin MII (alpha-Ctx

88 uccessfully used for treatment of opiate and nicotine addiction, but not for cocaine addiction.

89 ribute to the vulnerability or resiliency to nicotine addiction by altering the rewarding effects of

90 examine the role of mGluR5 downregulation in nicotine addiction by investigating a group of long-term

91 the ultimate nicotine delivery device; that nicotine addiction can be perpetuated and even enhanced

92 iched KEGG pathways in WBS children included nicotine addiction, cholesterol metabolism, arginine bio

93 one, belaperidone), malaria (mefloquine) and nicotine addiction (cytisine, varenicline).

94 Moreover, nicotine addiction drives repeated intake that results i

95 ased genome scanning studies for ethanol and nicotine addictions failed to display much agreement.

96 Australian families who participated in the Nicotine Addiction Genetics Project, 423 autosomal marke

97 entifying genetic factors that contribute to nicotine addiction has revealed several single nucleotid

98 ecognized very early, the modern concepts of nicotine addiction have relied on knowledge of cholinerg

99 immunotherapeutic approaches for cocaine and nicotine addiction have stimulated interest in creating

100 o encode reward and drive the development of nicotine addiction, however how nicotine alters a stress

101 gulin 3 (NRG3) and ErbB4 have been linked to nicotine addiction; however, the neuronal mechanisms and

102 , raising concerns about e-cigarette use and nicotine addiction in children.

103 might be protective against vulnerability to nicotine addiction in men.

104 d adjunctive sustained-release bupropion for nicotine addiction in patients with schizophrenia.

105 The prominence of nicotine addiction in schizophrenic patients is reflecte

106 e endgame would be an end to all tobacco and nicotine addiction in the United States, it supports fir

107 cal role of mGluR2/3 in different aspects of nicotine addiction, including acquisition and maintenanc

108 Nicotine addiction is a complex behavioral phenomenon co

109 Nicotine addiction is a major public health problem and

110 Nicotine addiction is a major public health problem, res

111 Nicotine addiction is associated with the development of

112 Nicotine addiction is characterized by repetitive drug t

113 Risk for alcohol and nicotine addiction is highly heritable, and they share c

114 A question relevant to nicotine addiction is how nicotine and other nicotinic r

115 Nicotine addiction is initiated by its binding to high-a

116 understanding of the bio-behavioral basis of nicotine addiction is needed.

117 stimuli) comorbid with the susceptibility to nicotine addiction is still poorly understood.

118 a formidable challenge for the treatment of nicotine addiction is the high vulnerability to relapse

119 review representative documents relating to nicotine addiction, low-tar, low-nicotine cigarettes, an

120 ence elevates nicotine's reward magnitude or nicotine addiction may rely more importantly upon negati

121 use, intensity of use (days per month), and nicotine addiction (measured as time after waking to fir

122 ex, variables related to smoking history and nicotine addiction, medical history, family history of l

123 psychopharmacological factors contribute to nicotine addiction, midbrain dopaminergic systems have r

124 Nicotine addiction (NA) is a common and devastating dise

125 7 subtypes to treat such diverse diseases as nicotine addiction, neuropathic pain, and neurodegenerat

126 es may play a role in the increased risk for nicotine addiction observed in adolescent offspring of s

127 provide efficient drug discovery methods for nicotine addiction or for other disorders that result fr

128 Along with solving a chemical mystery in nicotine addiction, our results provide guidance for eff

129 activation of this pathway may contribute to nicotine addiction, particularly in individuals with gen

130 the nicotine content of cigarettes to lower nicotine addiction potential in the United States.

131 Nicotine addiction progresses rapidly in adolescents and

132 nges underlying the NIC SST and SA and human nicotine addiction, providing a resource for understandi

133 smoking.SIGNIFICANCE STATEMENT Mechanisms of nicotine addiction remain poorly understood.

134 Nicotine addiction remains a major cause of disease and

135 ne presented to the brain over the course of nicotine addiction-shapes brain circuits that, among oth

136 an R336C substitution, have greater risk of nicotine addiction than non-carriers as assessed by the

137 ha4beta2 brain receptors thought to underlie nicotine addiction, the high affinity for nicotine is th

138 es, the tobacco industry striving to sustain nicotine addictions, the pharmaceutical industry to end

139 ed ion channel in the brain and a target for nicotine addiction therapy, and the 19-residue conotoxin

140 roach provides a new avenue for the field of nicotine addiction therapy.

141 sing numbers, Americans will seek to satisfy nicotine addictions through the use of novel nicotine-de

142 Nicotine addiction, through smoking, is the principal ca

143 Understanding the mechanisms underlying nicotine addiction to develop more effective treatment i

144 re needed to clarify the role of dopamine in nicotine addiction to help develop smoking prevention an

145 s pathophysiological conditions ranging from nicotine addiction to the development and progression of

146 This drug class should be considered for nicotine addiction treatment.

147 tum functional pathways may be effective for nicotine addiction treatment.

148 arly separated pathways that correlated with nicotine addiction vs nicotine's action were found.

149 odulator of habenular function that controls nicotine addiction vulnerability.

150 The severity of nicotine addiction was associated with the strength of d

151 stigations can elucidate the role of MORs in nicotine addiction, which may lead to development of nov

152 a possible biomarker for the early stages of nicotine addiction, with implications for its prevention

153 However, using nicotine replacement to treat nicotine addiction yields generally inconsistent results