- Browse by Subject
Browsing by Subject "cocaine"
Now showing 1 - 3 of 3
Results Per Page
Sort Options
Item Burden of Substance Abuse-Related Admissions to the Medical ICU(Elsevier, 2019) Westerhausen, Donald; Perkins, Anthony J.; Conley, Joshua; Khan, Babar A.; Farber, Mark; Biostatistics, School of Public HealthBackground Admissions to the ICU related to alcohol, prescription drugs, and illicit drugs are shown to be widespread and costly. In 1993, a study revealed 28% of ICU admissions at Johns Hopkins Hospital were related to substance abuse and accrued 39% of costs. Since then, health-care expenditures have increased, and substance abuse treatment admissions have risen. We conducted a study to provide updated data on ICU utilization and costs related to licit and illicit abuse at a large county hospital in Indianapolis, Indiana. Methods All admissions to the medical ICU at Eskenazi Hospital from March to October 2017 were reviewed. Demographics, reason for admission, relation to substance abuse and specific substance, ICU and hospital length of stay, Acute Physiology and Chronic Health Evaluation II (APACHE II) scores, mortality, insurance status, and hospital charges were collected based on chart review. Results A total of 611 admissions generated $74,587,280.35 in charges. A total of 25.7% of admissions related to substance abuse accounted for 23.1% of total charges. Illicit drugs were 13% of total admissions, generating 11% of charges. Alcohol-related admissions were 9.5% of total admissions, generating 7.6% of charges. Prescription drugs were 2.9% of admissions, generating 4.2% of charges. Of the substance abuse admissions, patients were generally men and 40 to 64 years of age, with longer ICU stay, higher APACHE II scores, and higher mortality. Conclusions Substance abuse admissions make up almost a one-quarter of resources used by our ICU. Patients tend to be younger and sicker with a higher risk of death. Identifying and accurately describing the landscape of this current health crisis will help us take appropriate action in the future.Item Caenorhabditis elegans as a Model to Study the Molecular and Genetic Mechanisms of Drug Addiction(Elsevier, 2016) Engleman, Eric A.; Katner, Simon N.; Neal-Beliveau, Bethany S.; Department of Psychiatry, IU School of MedicineDrug addiction takes a massive toll on society. Novel animal models are needed to test new treatments and understand the basic mechanisms underlying addiction. Rodent models have identified the neurocircuitry involved in addictive behavior and indicate that rodents possess some of the same neurobiologic mechanisms that mediate addiction in humans. Recent studies indicate that addiction is mechanistically and phylogenetically ancient and many mechanisms that underlie human addiction are also present in invertebrates. The nematode Caenorhabditis elegans has conserved neurobiologic systems with powerful molecular and genetic tools and a rapid rate of development that enables cost-effective translational discovery. Emerging evidence suggests that C. elegans is an excellent model to identify molecular mechanisms that mediate drug-induced behavior and potential targets for medications development for various addictive compounds. C. elegans emit many behaviors that can be easily quantitated including some that involve interactions with the environment. Ethanol (EtOH) is the best-studied drug-of-abuse in C. elegans and at least 50 different genes/targets have been identified as mediating EtOH's effects and polymorphisms in some orthologs in humans are associated with alcohol use disorders. C. elegans has also been shown to display dopamine and cholinergic system-dependent attraction to nicotine and demonstrate preference for cues previously associated with nicotine. Cocaine and methamphetamine have been found to produce dopamine-dependent reward-like behaviors in C. elegans. These behavioral tests in combination with genetic/molecular manipulations have led to the identification of dozens of target genes/systems in C. elegans that mediate drug effects. The one target/gene identified as essential for drug-induced behavioral responses across all drugs of abuse was the cat-2 gene coding for tyrosine hydroxylase, which is consistent with the role of dopamine neurotransmission in human addiction. Overall, C. elegans can be used to model aspects of drug addiction and identify systems and molecular mechanisms that mediate drug effects. The findings are surprisingly consistent with analogous findings in higher-level organisms. Further, model refinement is warranted to improve model validity and increase utility for medications development.Item Chronic Ethanol Drinking by Alcohol-preferring Rats Increases the Sensitivity of the Mesolimbic Dopamine System to the Reinforcing and Stimulating Effects of Cocaine(2013-08-20) Oster, Scott M.; Murphy, James M.; Rodd, Zachary A.; Goodlett, Charles R.; Kinzig, Kimberly P.; Czachowski, Cristine; Hazer, JohnAlcohol and cocaine are commonly co-abused drugs, and those meeting criteria for both cocaine and alcohol use disorders experience more severe behavioral and health consequences than those with a single disorder. Chronic alcohol (ethanol) drinking increased the reinforcing and dopamine (DA) neuronal stimulating effects of ethanol within mesolimbic regions of the central nervous system (CNS) of alcohol-preferring (P) rats. The objectives of the current study were to determine if chronic continuous ethanol drinking produced: (1) alterations in the sensitivity of the nucleus accumbens shell (AcbSh) to the reinforcing effects of cocaine, (2) changes in the magnitude and time course of the local stimulating effects of cocaine on posterior ventral tegmental area (pVTA) DA neurons, and (3) a persistence of alterations in the stimulating effects of cocaine after a period of protracted abstinence. Female P rats received continuous, free-choice access to water and 15% v/v ethanol for at least 10 wk (continuous ethanol-drinking; CE) or access to water alone (ethanol-naïve; N). A third group of rats received the same period of ethanol access followed by 30 d of protracted abstinence from ethanol (ethanol-abstinent; Ab). CE and Ab rats consumed, on average, 6-7 g/kg/d of ethanol. Animals with a single cannula aimed at the AcbSh responded for injections of cocaine into the AcbSh during four initial operant sessions. Cocaine was not present in the self-infused solution for the subsequent three sessions, and cocaine access was restored during one final session. Animals with dual ipsilateral cannulae aimed at the AcbSh and the pVTA were injected with pulsed microinfusions of cocaine into the pVTA while DA content was collected for analysis through a microdialysis probe inserted into the AcbSh. During the initial four sessions, neither CE nor N rats self-infused artificial cerebrospinal fluid (aCSF) or 0.1 mM cocaine into the AcbSh. CE, but not N, rats self-administered 0.5 mM cocaine into the AcbSh, whereas both groups self-infused concentrations of 1.0, 2.0, 4.0, or 8.0 mM cocaine. When cocaine access was restored in Session 8, CE rats responded more on the active lever and obtained more infusions of 0.5, 1.0, 2.0, or 4.0 mM cocaine compared to N rats. Microinjection of aCSF into the pVTA did not alter AcbSh DA levels in N, CE, or Ab rats. Microinjections of 0.25 mM cocaine into the pVTA did not significantly alter AcbSh DA levels in N animals, moderately increased DA levels in CE rats, and greatly increased DA levels in Ab rats. Microinjections of 0.5 mM cocaine into the pVTA modestly increased AcbSh DA levels in N animals, robustly increased DA levels in CE rats, and did not significantly alter DA levels in Ab rats. Microinjections of 1.0 or 2.0 mM cocaine into the pVTA modestly increased AcbSh DA levels in N animals but decreased DA levels in CE and Ab rats. Overall, long-term continuous ethanol drinking by P rats enhanced both the reinforcing effects of cocaine within the AcbSh and the stimulatory and inhibitory effects of cocaine on pVTA DA neurons. Alterations in the stimulatory and inhibitory effects of cocaine on pVTA DA neurons were not only enduring, but also enhanced, following a period of protracted abstinence from ethanol exposure. Translationally, prevention of chronic and excessive alcohol intake in populations with a genetic risk for substance abuse may reduce the likelihood of subsequent cocaine use.