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Background Synthetic cathinones are popularly referred to in the media as “bath salts.” Through the direct and indirect activation of the sympathetic nervous system, smoking, snorting, or injecting synthetic cathinones can result in tachycardia, hypertension, hyperthermia, myocardial infarction and death. Objectives The chemical structures and names of bath salts identified by the State of Ohio Bureau of Criminal Identification and Investigation Laboratory are presented. Based on their common pharmacophores the authors review the history, pharmacology, toxicology, detection methods and clinical implications of synthetic cathinones. Through the integration of this information, the pharmacological basis for the management of patients using synthetic cathinones is presented. Discussion Synthetic cathinones activate central serotonergic and dopaminergic systems contributing to acute psychosis and the peripheral activation of the sympathetic nervous system. The over stimulation of the sympathetic nervous system contributes to the many toxicities reported with bath salt use. The pharmacological basis for managing these patients is targeted at attenuating the activation of these systems. Conclusions Treatment of patients presenting after using bath salts should be focused on reducing agitation and psychosis, and supporting renal perfusion. The majority of successfully treated synthetic cathinones cases have used benzodiazepines and antipsychotics along with general supportive care.

Although it is widely accepted that alcohol abuse and alcoholism have a significant genetic component of risk, the identities of the genes themselves remain obscure. To illuminate such potential genetic contributions, DNA macroarrays were used to probe for differences in normative cortical gene expression between rat strains genetically selected for alcohol self-administration preference, AA (Alko, alcohol) and P (Indiana, preferring), or avoidance, ANA (Alko, nonalcohol) and NP (Indiana, nonpreferring). Among 1,176 genes studied, six demonstrated confirmable, differential expression following comparison of ethanol-naive AA and ANA rats. Specifically, the mRNA level for metabotropic glutamate receptor 3 (mGluR3) was down-regulated in the AA vs. ANA lines. In contrast, calcium channel subunit alpha2delta1 (cacna2d1), vesicle-associated membrane protein 2 (VAMP2), syntaxin 1 (both syntaxin 1a and 1b; STX1a and STX1b), and syntaxin binding protein (MUNC-18) mRNAs were found to be increased in frontal cortex following comparison of AA with ANA animals. Bioinformatic analysis of these molecular targets showed that mGluR3 and cacna2d1 fall within chromosomal locations reported to be alcohol-related by the Collaborative Study on the Genetics of Alcoholism (COGA) as well as quantitative trait loci (QTL) studies. To determine further whether these differences were strain specific, the above-mentioned genes were compared in ethanol-preferring (P) and -nonpreferring (NP) selected lines. VAMP2 was the only gene that displayed statistically different mRNA levels in a comparison of P and NP rats. In conclusion, the altered cortical gene expression illuminated here would have the effect of altering neurotransmitter release in AA rats (compared with ANA rats). Such alterations, however, might not be a universal characteristic of all animal models of alcohol abuse and will also require further investigation in post-mortem human samples.

Although functional genomic experiments (transcriptome analysis) have failed to identify a single alcoholism gene, they have illuminated important pathways and gene products that may contribute to the risk of alcohol abuse and alcoholism.

An open proteomic screen of serum and confirmation in a separate set of animals found Apo-AII to be increased in the serum of ethanol self-administering monkeys. These results are consistent with previous clinical studies of human ethanol consumption and serum apolipoprotein expression. Moreover, these results validate the use of non-human primates as a model organism for proteomic analysis of ethanol self-administration biomarkers.

In recent years, the human microbiome, or the collective term for all the microorganisms living on or within the human body (NIH Human Microbiome Project), has begun to emerge as a potential forensic tool. Forensically, the microbiome has the potential to be utilized as a unique identifier (Fierer et al., 2010;Oh et al., 2016), to link cohabiting individuals (Song et al., 2013), or to connect a person with a location and/or an object to a person (Yatsunenko et al., 2012).The successful use of the microbiome, regardless of the purpose, will

This article represents the proceedings of a workshop at the 2003 annual meeting of the Research Society on Alcoholism in Fort Lauderdale, FL. The workshop organizers/chairpersons were Chinnaswamy Kasinathan and Paul Manowitz. The presentations were (1) Introduction to the field of proteomics, by Kent Vrana; (2) Use of proteomics in the identification of urinary biomarkers for alcohol intake, by Chinnaswamy Kasinathan, Paul Thomas, and Paul Manowitz; (3) Proteomics screening illuminates ethanol-mediated induction of HDL proteins in macaques, by Kent Vrana, Randy Gooch, Travis Worst, Stephen Walker, Aaron Xu, Peter Pierre, Heather Green, and Kathleen Grant; and (4) Proteomics applied to the study of the liver, by Laura Beretta.