An overview of DNA methods for the identification and individualization of marijuana.
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The purpose of this review is to summarize the status of DNA-based methods for the identification and individualization of marijuana. In forensics, both identification of a substance as marijuana and the subsequent individualization of a sample may be desired for casework. Marijuana identification methods in the United States primarily include biochemical tests and, less frequently, DNA-based tests. Under special circumstances, DNA-based tests can be useful. For example, if the quantity of seized marijuana is extremely small and/or biochemical tests do not detect any D9-tetrahydrocannabinol (THC), DNA identification of plant material as Cannabis is still possible. This circumstance can arise when seeds, trace residue, tiny leaf fragments, or fine roots need to be analyzed. Methods for the individualization of marijuana include amplified fragment length polymorphism (AFLP), random amplified polymorphic DNA (RAPD), and short tandem repeat (STR) techniques that link an evidentiary sample to a source. Marijuana growers propagate their plants either by seed or by cloning. Seed-generated marijuana plants are expected to have unique DNA profiles analogous to a human population. Cloned marijuana plants, however, exhibit identical DNA profiles that allow for tracking of plant material derived from a common genetic lineage. The authors have validated the AFLP method for marijuana samples and are constructing a comparative database of marijuana seizure samples to estimate the expected frequency of a DNA profile match between unrelated plants. Continued development of DNA-based methods for plants can be useful for marijuana and other types of plant evidence in forensics. (+info)
Urinary cannabinoid detection times after controlled oral administration of delta9-tetrahydrocannabinol to humans.
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BACKGROUND: Urinary cannabinoid excretion and immunoassay performance were evaluated by semiquantitative immunoassay and gas chromatography-mass spectrometry (GC/MS) analysis of metabolite concentrations in 4381 urine specimens collected before, during, and after controlled oral administration of tetrahydrocannabinol (THC). METHODS: Seven individuals received 0, 0.39, 0.47, 7.5, and 14.8 mg THC/day in this double-blind, placebo-controlled, randomized, clinical study conducted on a closed research ward. THC doses (hemp oils with various THC concentrations and the therapeutic drug Marinol) were administered three times daily for 5 days. All urine voids were collected over the 10-week study and later tested by Emit II, DRI, and CEDIA immunoassays and by GC/MS. Detection rates, detection times, and sensitivities, specificities, and efficiencies of the immunoassays were determined. RESULTS: At the federally mandated immunoassay cutoff (50 microg/L), mean detection rates were <0.2% during ingestion of the two low doses typical of current hemp oil THC concentrations. The two high doses produced mean detection rates of 23-46% with intermittent positive tests up to 118 h. Maximum metabolite concentrations were 5.4-38.2 microg/L for the low doses and 19.0-436 micro g/L for the high doses. Emit II, DRI, and CEDIA immunoassays had similar performance efficiencies of 92.8%, 95.2%, and 93.9%, respectively, but differed in sensitivity and specificity. CONCLUSIONS: The use of cannabinoid-containing foodstuffs and cannabinoid-based therapeutics, and continued abuse of oral cannabis require scientific data for accurate interpretation of cannabinoid tests and for making reliable administrative drug-testing policy. At the federally mandated cannabinoid cutoffs, it is possible but unlikely for a urine specimen to test positive after ingestion of manufacturer-recommended doses of low-THC hemp oils. Urine tests have a high likelihood of being positive after Marinol therapy. The Emit II and DRI assays had adequate sensitivity and specificity, but the CEDIA assay failed to detect many true-positive specimens. (+info)
Secretory vesicle formation in the secretory cavity of glandular trichomes of Cannabis sativa L. (Cannabaceae).
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The disc cell wall facing the secretory cavity in lipophilic glands of Cannabis was studied for origin and distribution of hyaline areas, secretory vesicles, fibrillar matrix and particulate material. Secretions evident as light areas in the disc cell cytoplasm pass through modified regions in the plasma membrane and appear as hyaline areas in the cell wall. Hyaline areas, surrounded with a filamentous outline, accumulate near the wall surface facing the secretory cavity where they fuse to form enlarged hyaline areas. Fibrillar matrix is related to and may originate from the dense outer layer of the plasma membrane. This matrix becomes distributed throughout the wall material and contributes in part to the composition of the surface feature of secretory vesicles. Thickening of the cell wall is associated with secretions from the disc cells that facilitates movement of hyaline areas, fibrillar matrix and other possible secretions through the wall to form secretory vesicles and intervesicular materials in the secretory cavity. The outer wall of disc cells in aggregate forms the basilar wall surface of the secretory cavity which facilitates the organization of secretory vesicles that fill the secretory cavity. (+info)
Interaction of adrenergic antagonists with prostaglandin E2 and tetrahydrocannabinol in the eye.
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Both alpha- and beta-adrenergic antagonists have been utilized in an atempt to discern the site of action of prostaglandin (PG) and tetrahydrocannabinol (THC) in the eye. Both alpha- and beta-adrenergic antagonists (alpha-antagonists, phentolamine and phenoxybenzamine; beta-antagonists, propranolol and sotalol) cuased a dose-dependent reduction in intraocular pressure and blood pressure and increased total outflow facility. The results are consistent with the concept that both alpha- and beta-adrenergic receptors are present in the anterior uvea and that vasomotor tone is essential to the maintenance of normal intraocular pressure. No antagonist reduced the PG-induced elevation of intraocular pressure unless the blood pressure was severely lowered. All antagonists inhibit the normal PG-induced increase in total outflow facility, indicating that these agents protect the blood-aqueous barrier from breakdown without altering the vasodilatory response to PG. All antagonists reduced the fall in intraocular pressure produced by THC by approximately 50 per cent, except for sotalol which completely abolished the intraocular pressure fall. Only the alpha-adrenergic antagonists prevented the THC-induced increase in total outflow facility. The results indicate that true outflow facility may well be regulated exclusively by alpha-receptors. The data are consistent with the effect of THC being primarily a vasodilation of the efferent blood vessels of the anterior uvea. The partial inhibition by alpha-adrenergic antagonists may also suggest a lesser role of THC on the afferent vessels. (+info)
Marijuana withdrawal in humans: effects of oral THC or divalproex.
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Abstinence following daily marijuana use can produce a withdrawal syndrome characterized by negative mood (eg irritability, anxiety, misery), muscle pain, chills, and decreased food intake. Two placebo-controlled, within-subject studies investigated the effects of a cannabinoid agonist, delta-9-tetrahydrocannabinol (THC: Study 1), and a mood stabilizer, divalproex (Study 2), on symptoms of marijuana withdrawal. Participants (n=7/study), who were not seeking treatment for their marijuana use, reported smoking 6-10 marijuana cigarettes/day, 6-7 days/week. Study 1 was a 15-day in-patient, 5-day outpatient, 15-day in-patient design. During the in-patient phases, participants took oral THC capsules (0, 10 mg) five times/day, 1 h prior to smoking marijuana (0.00, 3.04% THC). Active and placebo marijuana were smoked on in-patient days 1-8, while only placebo marijuana was smoked on days 9-14, that is, marijuana abstinence. Placebo THC was administered each day, except during one of the abstinence phases (days 9-14), when active THC was given. Mood, psychomotor task performance, food intake, and sleep were measured. Oral THC administered during marijuana abstinence decreased ratings of 'anxious', 'miserable', 'trouble sleeping', 'chills', and marijuana craving, and reversed large decreases in food intake as compared to placebo, while producing no intoxication. Study 2 was a 58-day, outpatient/in-patient design. Participants were maintained on each divalproex dose (0, 1500 mg/day) for 29 days each. Each maintenance condition began with a 14-day outpatient phase for medication induction or clearance and continued with a 15-day in-patient phase. Divalproex decreased marijuana craving during abstinence, yet increased ratings of 'anxious', 'irritable', 'bad effect', and 'tired.' Divalproex worsened performance on psychomotor tasks, and increased food intake regardless of marijuana condition. Thus, oral THC decreased marijuana craving and withdrawal symptoms at a dose that was subjectively indistinguishable from placebo. Divalproex worsened mood and cognitive performance during marijuana abstinence. These data suggest that oral THC, but not divalproex, may be useful in the treatment of marijuana dependence. (+info)
Extract from Fructus cannabis activating calcineurin improved learning and memory in mice with chemical drug-induced dysmnesia.
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AIM: To investigate the effects of extract from Fructus cannabis (EFC) that can activate calcineurin on learning and memory impairment induced by chemical drugs in mice. METHODS: Bovine brain calcineurin and calmodulin were isolated from frozen tissues. The activity of calcineurin was assayed using p-nitrophenyl phosphate (PNPP) as the substrate. Step-down type passive avoidance test and water maze were used together to determine the effects of EFC on learning and memory dysfunction. RESULTS: EFC activated calcineurin activity at a concentration range of 0.01-100 g/L. The maximal value of EFC on calcineurin activity (35 %+/-5 %) appeared at a concentration of 10 g/L. The chemical drugs such as scopolamine, sodium nitrite, and 45 % ethanol, and sodium pentobarbital induced learning and memory dysfunction. EFC administration (0.2, 0.4, and 0.8 g/kg, igx7 d) prolonged the latency and decreased the number of errors in the step-down test. EFC, given for 7 d, enhanced the spatial resolution of amnesic mice in water maze test. EFC overcome amnesia of three stages of memory process at the dose of 0.2 g/kg. CONCLUSION: EFC with an activation role of calcineurin can improve the impaired learning and memory induced by chemical drugs in mice. (+info)
A case of cannabis-induced pancreatitis.
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CONTEXT: There are no previous reports of acute pancreatitis associated with cannabis use in the general population. Drugs of all types are related to the aetiology of pancreatitis in approximately 1.4-2.0% of cases. CASE REPORT: We report the case of a 29 year old man who presented with acute pancreatitis after a period of heavy cannabis smoking. Other causes of the disease were ruled out. The pancreatitis resolved itself after the cannabis was stopped and this was confirmed by urinary cannabinoid metabolite monitoring in the community. CONCLUSION: To our knowledge this is the first description of a case of cannabis induced pancreatitis. However, the link is difficult to establish and further evidence is required to prove the association. (+info)
Causal association between cannabis and psychosis: examination of the evidence.
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BACKGROUND: Controversy remains as to whether cannabis acts as a causal risk factor for schizophrenia or other functional psychotic illnesses. AIMS: To examine critically the evidence that cannabis causes psychosis using established criteria of causality. METHOD: We identified five studies that included a well-defined sample drawn from population-based registers or cohorts and used prospective measures of cannabis use and adult psychosis. RESULTS: On an individual level, cannabis use confers an overall twofold increase in the relative risk for later schizophrenia. At the population level, elimination of cannabis use would reduce the incidence of schizophrenia by approximately 8%, assuming a causal relationship. Cannabis use appears to be neither a sufficient nor a necessary cause for psychosis. It is a component cause, part of a complex constellation of factors leading to psychosis. CONCLUSIONS: Cases of psychotic disorder could be prevented by discouraging cannabis use among vulnerable youths. Research is needed to understand the mechanisms by which cannabis causes psychosis. (+info)