910 resultados para Cannabis dependence
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Origin of samples of Cannabis sativa through insect fragments associated with compacted hemp drug in South America. Insects associated with a seizure of Cannabis sativa L. may indicate the origin of the illicit drug. Nevertheless, no work regarding this subject has been previously published for South America. In the present investigation, seven kilograms of vegetal material (C. sativa) were inspected for insect fragments. Three species were identified and used to test the origin of the seizure of cannabis plant material: Euschistus heros (Fabricius, 1794), Thyanta perditor (Fabricius, 1794) (Heteroptera, Pentatomidae), and Cephalotes pusillus (Klug, 1824) (Hymenoptera, Formicidae). These insect species restricted the geographic origin of the drug to the Neotropical region, and their distribution patterns showed an overlap of the State of Mato Grosso (Brazil), Argentina, and Paraguay. Based on this information, two of the three major C. sativa growing areas in South America were excluded: (1) the Colombian territory and (2) northeastern Brazil.
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BACKGROUND: Interventions have been developed to reduce overestimations of substance use among others, especially for alcohol and among students. Nevertheless, there is a lack of knowledge on misperceptions of use for substances other than alcohol. We studied the prevalence of misperceptions of use for tobacco, cannabis, and alcohol and whether the perception of tobacco, cannabis, and alcohol use by others is associated with one's own use. METHODS: Participants (n=5216) in a cohort study from a census of 20-year-old men (N=11,819) estimated the prevalence of tobacco and cannabis use among peers of the same age and sex and the percentage of their peers drinking more alcohol than they did. Using the census data, we determined whether participants overestimated, accurately estimated, or underestimated substance use by others. Regression models were used to compare substance use by those who overestimated or underestimated peer substance with those who accurately estimated peer use. Other variables included in the analyses were the presence of close friends with alcohol or other drug problems and family history of substance use. RESULTS: Tobacco use by others was overestimated by 46.1% and accurately estimated by 37.3% of participants. Cannabis use by others was overestimated by 21.8% and accurately estimated by 31.6% of participants. Alcohol use by others was overestimated by more than half (53.4%) of participants and accurately estimated by 31.0%. In multivariable models, compared with participants who accurately estimated tobacco use by others, those who overestimated it reported smoking more cigarettes per week (incidence rate ratio [IRR] [95% CI], 1.17 [range, 1.05, 1.32]). There was no difference in the number of cigarettes smoked per week between those underestimating and those accurately estimating tobacco use by others (IRR [95% CI], 0.99 [range, 0.84, 1.17]). Compared with participants accurately estimating cannabis use by others, those who overestimated it reported more days of cannabis use per month (IRR [95% CI], 1.43 [range, 1.21, 1.70]), whereas those who underestimated it reported fewer days of cannabis use per month (IRR [95% CI], 0.62 [range, 0.23, 0.75]). Compared with participants accurately estimating alcohol use by others, those who overestimated it reported consuming more drinks per week (IRR [95% CI], 1.57 [range, 1.43, 1.72]), whereas those who underestimated it reported consuming fewer drinks per week (IRR [95% CI], 0.41 [range, 0.34, 0.50]). CONCLUSIONS: Perceptions of substance use by others are associated with one's own use. In particular, overestimating use by others is frequent among young men and is associated with one's own greater consumption. This association is independent of the substance use environment, indicating that, even in the case of proximity to a heavy-usage group, perception of use by others may influence one's own use. If preventive interventions are to be based on normative feedback, and their aim is to reduce overestimations of use by others, then the prevalence of overestimation indicates that they may be of benefit to roughly half the population; or, in the case of cannabis, to as few as 20%. Such interventions should take into account differing strengths of association across substances.
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Cannabis use is highly prevalent among people with schizophrenia, and coupled with impaired cognition, is thought to heighten the risk of illness onset. However, while heavy cannabis use has been associated with cognitive deficits in long-term users, studies among patients with schizophrenia have been contradictory. This article consists of 2 studies. In Study I, a meta-analysis of 10 studies comprising 572 patients with established schizophrenia (with and without comorbid cannabis use) was conducted. Patients with a history of cannabis use were found to have superior neuropsychological functioning. This finding was largely driven by studies that included patients with a lifetime history of cannabis use rather than current or recent use. In Study II, we examined the neuropsychological performance of 85 patients with first-episode psychosis (FEP) and 43 healthy nonusing controls. Relative to controls, FEP patients with a history of cannabis use (FEP + CANN; n = 59) displayed only selective neuropsychological impairments while those without a history (FEP - CANN; n = 26) displayed generalized deficits. When directly compared, FEP + CANN patients performed better on tests of visual memory, working memory, and executive functioning. Patients with early onset cannabis use had less neuropsychological impairment than patients with later onset use. Together, these findings suggest that patients with schizophrenia or FEP with a history of cannabis use have superior neuropsychological functioning compared with nonusing patients. This association between better cognitive performance and cannabis use in schizophrenia may be driven by a subgroup of "neurocognitively less impaired" patients, who only developed psychosis after a relatively early initiation into cannabis use.
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Malgré une récente réduction, le tabagisme reste élevé et préoccupant parmi les jeunes. Les consommations de tabac et de cannabis sont, sur plusieurs aspects, fortement liées. Les preuves scientifiques tendent à démontrer que la dépendance à la nicotine et la consommation persistante de cigarettes seraient les deux principales conséquences néfastes de l'usage de cannabis pendant l'adolescence. Le phénomène du "mulling" (le fait de mélanger du tabac au cannabis pour sa consommation) représente l'une des hypothèses les plus plausibles du risque augmenté qu'ont les jeunes consommateurs de cannabis de devenir des futurs fumeurs de cigarettes. L'objectif principal de cette étude est de déterminer si les niveaux de nicotine retrouvés chez des fumeurs de cannabis sont suffisamment élevés pour prouver une exposition tabagique significative pouvant être expliquée par le phénomène du "mulling" plutôt que par l'environnement.
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Two retrospective epidemiologic studies have shown that cannabis is the main psychoactive substance detected in the blood of drivers suspected of driving under the influence of psychotropic drugs. An oral administration double-blind crossover study was carried out with eight healthy male subjects, aged 22 to 30 years, all occasional cannabis smokers. Three treatments and one placebo were administered to all participants at a two week interval: 20 mg dronabinol, 16.5 mg D9-tétrahydrocannabinol (THC) and 45.7 mg THC as a cannabis milk decoction. Participants were asked to report the subjective drug effects and their willingness to drive under various circumstances on a visual analog scale. Clinical observations, a psychomotor test and a tracking test on a driving simulator were also carried out. Compared to cannabis smoking, THC, 11-OH-THC and THC-COOH blood concentrations remained low through the whole study (<13.1 ng THC/mL,<24.7 ng 11-OH-THC/mL and<99.9 ng THC-COOH/mL). Two subjects experienced deep anxiety symptoms suggesting that this unwanted side-effect may occur when driving under the influence of cannabis or when driving and smoking a joint. No clear association could be found between these adverse reactions and a susceptibility gene to propensity to anxiety and psychotic symptoms (genetic polymorphism of the catechol-O-methyltransferase). The questionnaires have shown that the willingness to drive was lower when the drivers were assigned an insignificant task and was higher when the mission was of crucial importance. The subjects were aware of the effects of cannabis and their performances on the road sign and tracking test were greatly impaired, especially after ingestion of the strongest dose. The Cannabis Influence Factor (CIF) which relies on the molar ratio of active and inactive cannabinoids in blood provided a good estimate of the fitness to drive.
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MAP5, a microtubule-associated protein characteristic of differentiating neurons, was studied in the developing visual cortex and corpus callosum of the cat. In juvenile cortical tissue, during the first month after birth, MAP5 is present as a protein doublet of molecular weights of 320 and 300 kDa, defined as MAP5a and MAP5b, respectively. MAP5a is the phosphorylated form. MAP5a decreases two weeks after birth and is no longer detectable at the beginning of the second postnatal month; MAP5b also decreases after the second postnatal week but more slowly and it is still present in the adult. In the corpus callosum only MAP5a is present between birth and the end of the first postnatal month. Afterwards only MAP5b is present but decreases in concentration more than 3-fold towards adulthood. Our immunocytochemical studies show MAP5 in somata, dendrites and axonal processes of cortical neurons. In adult tissue it is very prominent in pyramidal cells of layer V. In the corpus callosum MAP5 is present in axons at all ages. There is strong evidence that MAP5a is located in axons while MAP5b seems restricted to somata and dendrites until P28, but is found in callosal axons from P39 onwards. Biochemical experiments indicate that the state of phosphorylation of MAP5 influences its association with structural components. After high speed centrifugation of early postnatal brain tissue, MAP5a remains with pellet fractions while most MAP5b is soluble. In conclusion, phosphorylation of MAP5 may regulate (1) its intracellular distribution within axons and dendrites, and (2) its ability to interact with other subcellular components.
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This paper summarizes data on the factors involved in addiction and dependence to cigarettes. Nicotine has been intensively studied by the tobacco industry, for instance for its addictive effect at the lowest possible rates. The addition of diammonium phosphate and urea produces an alcalinization of the pH of cigarette smoke, and promotes the absorption and the trans-membrane passage of nicotine. The taste, the smell of smoke, and the visual aspect of the pack of cigarettes are also sensory components that promote addiction. Finally, menthol, sugar, cocoa and liquorice added to cigarettes also play a role in dependence and addiction to cigarettes by, for instance, making an anesthetic effect on the airways.
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PURPOSE: To assess tobacco, alcohol, cannabis and benzodiazepine use in methadone maintenance treatment (MMT) as potential sources of variability in methadone pharmacokinetics. METHODS: Trough plasma (R)- and (S)-methadone concentrations were measured on 77 Australian and 74 Swiss MMT patients with no additional medications other than benzodiazepines. Simple and multiple regression analyses were performed for the primary metric, plasma methadone concentration/dose. RESULTS: Cannabis and methadone dose were significantly associated with lower 24-h plasma (R)- and (S)-methadone concentrations/dose. The models containing these variables explained 14-16% and 17-25% of the variation in (R)- and (S)-methadone concentration/dose, respectively. Analysis of 61 patients using only CYP3A4 metabolised benzodiazepines showed this class to be associated with higher (R)-concentration/dose, which is consistent with a potential competitive inhibition of CYP3A4. CONCLUSION: Cannabis use and higher methadone doses in MMT could in part be a response to-or a cause of-more rapid methadone clearance. The effects of cannabis and benzodiazepines should be controlled for in future studies on methadone pharmacokinetics in MMT.
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BACKGROUND/AIMS: Cannabis use is a growing challenge for public health, calling for adequate instruments to identify problematic consumption patterns. The Cannabis Use Disorders Identification Test (CUDIT) is a 10-item questionnaire used for screening cannabis abuse and dependency. The present study evaluated that screening instrument. METHODS: In a representative population sample of 5,025 Swiss adolescents and young adults, 593 current cannabis users replied to the CUDIT. Internal consistency was examined by means of Cronbach's alpha and confirmatory factor analysis. In addition, the CUDIT was compared to accepted concepts of problematic cannabis use (e.g. using cannabis and driving). ROC analyses were used to test the CUDIT's discriminative ability and to determine an appropriate cut-off. RESULTS: Two items ('injuries' and 'hours being stoned') had loadings below 0.5 on the unidimensional construct and correlated lower than 0.4 with the total CUDIT score. All concepts of problematic cannabis use were related to CUDIT scores. An ideal cut-off between six and eight points was found. CONCLUSIONS: Although the CUDIT seems to be a promising instrument to identify problematic cannabis use, there is a need to revise some of its items.
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PURPOSE: Recently, a 76-gene prognostic signature able to predict distant metastases in lymph node-negative (N(-)) breast cancer patients was reported. The aims of this study conducted by TRANSBIG were to independently validate these results and to compare the outcome with clinical risk assessment. EXPERIMENTAL DESIGN: Gene expression profiling of frozen samples from 198 N(-) systemically untreated patients was done at the Bordet Institute, blinded to clinical data and independent of Veridex. Genomic risk was defined by Veridex, blinded to clinical data. Survival analyses, done by an independent statistician, were done with the genomic risk and adjusted for the clinical risk, defined by Adjuvant! Online. RESULTS: The actual 5- and 10-year time to distant metastasis were 98% (88-100%) and 94% (83-98%), respectively, for the good profile group and 76% (68-82%) and 73% (65-79%), respectively, for the poor profile group. The actual 5- and 10-year overall survival were 98% (88-100%) and 87% (73-94%), respectively, for the good profile group and 84% (77-89%) and 72% (63-78%), respectively, for the poor profile group. We observed a strong time dependence of this signature, leading to an adjusted hazard ratio of 13.58 (1.85-99.63) and 8.20 (1.10-60.90) at 5 years and 5.11 (1.57-16.67) and 2.55 (1.07-6.10) at 10 years for time to distant metastasis and overall survival, respectively. CONCLUSION: This independent validation confirmed the performance of the 76-gene signature and adds to the growing evidence that gene expression signatures are of clinical relevance, especially for identifying patients at high risk of early distant metastases.
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It is well known that exposure to low doses of lead causes long-lasting neurobehavioural deficits, but the cellular changes underlying these behavioural changes remain to be elucidated. A protective role of glial cells on neurons through lead sequestration by astrocytes has been proposed. The possible modulation of lead neurotoxicity by neuron-glia interactions was examined in three-dimensional cultures of foetal rat telencephalon. Mixed-brain cell cultures or cultures enriched in either neurons or glial cells were treated for 10 days with lead acetate (10(-6) m), a concentration below the limit of cytotoxicity. Intracellular lead content and cell type-specific enzyme activities were determined. It was found that in enriched cultures neurons stored more lead than glial cells, and each cell type alone stored more lead than in co-culture. Moreover, glial cells but not neurons were more affected by lead in enriched culture than in co-culture. These results show that neuron-glia interactions attenuate the cellular lead uptake and the glial susceptibility to lead, but they do not support the idea of a protective role of astrocytes.