Notes

Acting talk generator development along with apraxia involving speech from the DIVA/GODIVA neurocomputational platform.
After ≥1 year frozen storage, 80.7% of laboratory specimens positive for THC (3 ng/mL cut-off) by GC-MS were reconfirmed positive (within 25%), with an average THC decrease of 4.2%. Specimens (n = 47) processed with Oral-Eze (diluted) and tested via enzyme immunoassay were concordant with LC-MS-MS results and showed 100% sensitivity and 95% specificity. Paired specimens collected with Oral-Eze and Intercept exhibited 98% overall agreement between the immunoassay test systems. Collectively, these data demonstrate consistent and reproducible recovery and stability of THC in OF after collection, transport and laboratory testing using the Oral-Eze OF Collection System.This article reviews case reports for 58 suspected impaired driving cases that were positive for the synthetic cannabinoids AB-CHMINACA or AB-PINACA. All cases were submitted to the Washington State Patrol Toxicology Laboratory in 2014 from either Washington State or State of Alaska law enforcement agencies. The population of drivers was predominantly male (95%), with a mean age of 28 years (range, 18-61 years). The range of blood concentrations was 0.6->10 ng/mL for AB-CHMINACA (N = 33) and 0.6-41.3 ng/mL for AB-PINACA (N = 25). Drug Recognition Expert exams were performed in 10 cases for each AB-CHMINACA and AB-PINACA. Horizontal gaze nystagmus was observed in 50 and 60% of the cases, respectively. Overall, several physiological indicators varied from those typically observed with marijuana use. The majority of these cases had very poor driving; subjects were involved in an accident, found passed out in a vehicle or were called in as a suspected impaired driver. Slurred speech, confusion, lack of coordination/dexterity and lethargy were commonly observed.Paroxetine is a selective serotonin reuptake inhibitor commonly prescribed for the treatment of depression, obsessive-compulsive disorder, panic disorder, social anxiety disorder and post-traumatic stress disorder. While the use of paroxetine is considered relatively safe, negative side effects, including nausea, drowsiness, insomnia and dizziness, can adversely affect a pilot's ability to safely operate an aircraft. The use of paroxetine may increase suicidal behavior and suicidal ideation. When relying on postmortem specimens for toxicological evaluation, a general understanding of drug distribution throughout postmortem specimens is important. This laboratory has determined the distribution of paroxetine in postmortem tissues and fluids from nine aviation accident fatalities. Specimens were processed using an n-butyl chloride liquid/liquid extraction followed by gas chromatographic/mass spectrometeric analysis. Blood paroxetine concentrations obtained from these cases ranged from 0.019 to 0.865 µg/mL. The distribution of paroxetine, expressed as mean specimen/blood ratio, was 1.67 ± 1.16 urine (n = 4), 0.08 ± 0.04 vitreous humor (n = 6), 5.77 ± 1.37 liver (n = 8), 9.66 ± 2.58 lung (n = 9), 1.44 ± 0.57 kidney (n = 8), 3.80 ± 0.69 spleen (n = 8), 0.15 ± 0.04 muscle (n = 8), 4.27 ± 2.64 brain (n = 7) and 1.05 ± 0.43 heart (n = 8). The large standard deviations associated with the paroxetine distribution coefficients suggest that paroxetine can experience significant postmortem concentration changes.The North Carolina Office of the Chief Medical Examiner Toxicology Laboratory identified 61 cases from 2002 to 2014 where metaxalone was detected during routine postmortem drug screening in support of a determination of cause and manner of death. Decedents were divided into groups based on the manner of death with the goal of studying metaxalone concentrations in overdose and non-overdose situations (natural, accident, suicide and undetermined). Subgroups were established for cases in which metaxalone contributed to the cause of death (attributed) and cases in which it did not (unattributed). Attributed cases were divided into those where metaxalone additively combined with other drugs and cases in which the drug was present in sufficient amounts to be the primary cause of death, regardless of other drugs present and the concentrations of those drugs. The mean metaxalone concentration for the additive deaths was 14.2 mg/L with a median value of 11 mg/L (n = 18) and a mean metaxalone concentration of 36.7 mg/L with a median value of 32 mg/L (n = 9) for primary deaths. For unattributed metaxalone concentrations, the mean was 3.4 mg/L with a median value of 2.9 mg/L (n = 31). Of the 61 cases, 34% fall at or below a therapeutic concentration of ≤4 mg/L. The selected case studies offer valuable information regarding postmortem interpretation.Nails (fingernails and toenails) are made of keratin. As the nail grows, substances incorporate into the keratin fibers where they can be detected 3-6 months after use. Samples are collected by clipping of 2-3 mm of nail from all fingers (100 mg). We present drug testing results from 10,349 nail samples collected from high-risk cases during a 3-year period of time. Samples were analyzed by validated analytical methods. The initial testing was performed mostly using enzyme-linked immunosorbent assay, but by liquid chromatography-tandem mass spectrometry (LC-MS-MS) as well. Presumptive positive samples were subjected to confirmatory testing with sample preparation procedures including washing, pulverizing, digestion and extraction optimized for each drug class. The total of 7,799 samples was analyzed for amphetamines. The concentrations ranged from 40 to 572,865 pg/mg (median, 100-3,687) for all amphetamine analytes. Amphetamine and methamphetamine were present in 14% of the samples, 22 samples were positive fotechniques are simple and produce accurate and precise results. Sensitive analytical instrumentation, mainly LC-MS-MS, allows for detection of femtogram (10(-15) g) quantities of substances in nails. Samples were from a high-risk population, therefore the extraordinary positivity rate was observed.In recent years, N-methoxybenzyl-methoxyphenylethylamine (NBOMe) derivatives, a class of designer hallucinogenic drugs, have become popular drugs of abuse. These drugs have been the cause of severe intoxications and even deaths. They act as 5-HT2A receptors agonists and have been reported to produce serotonin-like syndrome with bizarre behavior, severe agitation and seizures persisting for as long as 3 days. The most commonly reported derivatives are 25I-NBOMe, 25B-NBOMe and 25C-NBOMe, respectively 2-(4-iodo-2,5-dimethoxyphenyl)-N-[(2-methoxyphenyl) methyl]ethanamine, N-(2-methoxybenzyl)-2,5-dimethoxy-4-bromophenethylamine and N-(2-methoxybenzyl)-2,5-dimethoxy-4-chlorophenethylamine. Like many low dose hallucinogenic drugs these compounds are often sold on blotter paper. Three different types of commercially available blotter papers reported to contain NBOMe derivatives were obtained. These blotter papers were screened using Direct Analysis in Real Time AccuTOF(TM) mass spectrometry followed by confirmation and quantification by high-performance liquid chromatography triple quadrapole mass spectrometry. The major drug present on each of the three blotter products was different, 25I-NBOMe, 25C-NBOMe or 25B-NBOMe. The blotter papers were also found to have minute amounts of two or three NBOMe derivative impurities of 25H-NBOMe, 25I-NBOMe, 25C-NBOMe, 25B-NBOMe and/or 25D-NBOMe.'NBOMe' (dimethoxyphenyl-N-[(2-methoxyphenyl)methyl]ethanamine) derivatives are a new class of designer hallucinogenic drugs widely available on the Internet. Currently, 2-(4-iodo-2,5-dimethoxyphenyl)-N-[(2-methoxyphenyl)methyl]ethanamine (25I-NBOMe) is the most popular abused derivative in the USA. There are little published data on the absorption, metabolism and elimination of 25I-NBOMe, or any of the other NBOMe derivatives. Therefore, there are no definitive metabolite biomarkers. We present the identification of fifteen 25I-NBOMe metabolites in phase I and II mouse hepatic microsomal preparations, and analysis of two human urine samples from 25I-NBOMe-intoxicated patients to test the utility of these metabolites as biomarkers of 25I-NBOMe use. The synthesis of two major urinary metabolites, 2-iodo-4-methoxy-5-[2-[(2-methoxyphenyl) methylamino]ethyl]phenol (2-O-desmethyl-5-I-NBOMe, M5) and 5-iodo-4-methoxy-2-[2-[(2-methoxyphenyl)methylamino]ethyl]phenol (5-O-desmethyl-2-I-NBOMe), is also presented. Seven phase II glucuronidated metabolites of the O-desmethyl or the hydroxylated phase I metabolites were identified. One human urine sample contained 25I-NBOMe as well as all 15 metabolites identified in mouse hepatic microsomal preparations. Another human urine sample contained no parent 25I-NBOMe, but was found to contain three O-desmethyl metabolites. We recommend β-glucuronidase enzymatic hydrolysis of urine prior to 25I-NBOMe screening and the use of M5 as the primary biomarker in drug testing.Over the last few years, NBOMe substances have been used either as a legal alternative to lysergic acid diethylamide (LSD) or sold surreptitiously as LSD to unknown users. These NBOMe substances have been detected in blotter papers, powders, capsules and liquids. We report the deaths of two teenage male subjects that were related to 25B-NBOMe and 25I-NBOMe in Indiana during 2014. Samples were extracted via a solvent protein precipitation with acetonitrile and analyzed via ultra-performance liquid chromatography with tandem mass spectrometry. For these two cases, we describe the NBOMe instrumental analysis, toxicological results for postmortem heart blood and urine specimens and the relevant case history and pathological findings at autopsy. In the first case, 25B-NBOMe was detected in postmortem heart blood at 1.59 ng/mL; in the second case, 25I-NBOMe was detected in postmortem heart blood at 19.8 ng/mL. We also review relevant published casework from clinical toxicology and postmortem toxicology in which analytically confirmed 25B-NBOMe and 25I-NBOMe were determined to be causative agents in intoxications or deaths.Cannabis intoxication in living and deceased drivers is an important medico-legal topic, but only a limited number of studies examine cannabinoids in living and deceased humans. This study compares cannabinoid concentrations (in ng/mL) in driving under the influence of drug (DUID) drivers with blood cannabinoids to those in drivers who died while driving with cannabinoids in their postmortem (PM) peripheral blood. From 2010 to 2013, there were 318 cannabis-positive DUID cases (mean, median THC 4.9, 3); 88 had cannabis-only in their bloods (mean, median THC 5.8, 4). In 23 DUID cases, Huestis' Predictive Models with 95% confidence intervals were applied and evaluated, demonstrating that the actual case time points in all 23 cases fell within the predicted time ranges. Among deceased drivers, 19 had cannabis-positive toxicology (mean, median THC 11.7, 4.5) and 8 had cannabis-only (mean, median THC 20.3, 19.5). Motorcyclists and bicyclists comprised the majority of deceased vehicle operators, with bicyclists averaging the highest mean and median THC concentrations overall. click here The analysis of variance between living and deceased drivers' cannabinoid concentrations showed that THC-OH and THC-COOH concentrations are not statistically different between the two groups, but that THC concentrations are statistically different, making it difficult to directly correlate PM with antemortem THC concentrations between living and deceased drivers.
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